Objective To discuss the effect of Jiegeng Yuanshen Tang（JGYST） on airway tissue inflammation and mucus secretion in the mice with allergic asthma， and to clarify the related mechanism. Methods Forty male C57BL/J mice were randomly divided into control group， JGYST group， ovalbumin （OVA） group， and OVA + JGYST group. The mice in OVA group and OVA +JGYST group were sensitized with 50 μg OVA via intraperitoneal injection twice weekly， followed by 20 μg OVA nasal drops daily for 7 d to induce asthma；the mice in OVA +JGYST group were gavaged with 200 μL JGYST 1 h before each OVA challenge， and the administration lasted for 7 d； the mice in control group were given equivalent dose of PBS via intraperitoneal injection， nasal drops， and gavage； the mice in JGYST group were given the same dose of PBS for intraperitoneal and nasal administration and gavaged with the same dose of JGYST. The pathomorphology of lung tissue of the mice in various groups was observed by HE staining and periodic acid-Schiff （PAS） staining， and the inflammation and PAS scores were calculated； flow cytometry method was used to detect the numbers of eosinophils， neutrophils， helper T lymphocyte 1 （Th1） cells， helper T lymphocyte 2 （Th2） cells， and dendritic cells （DCs）， as well as the percentage of mature DCs and level of reactive oxygen species （ROS） in lung tissue of the mice in various groups；real-time fluorescence quantitative PCR （RT-qPCR） method was used to detect the expression levels of interleukin-4 （IL-4）， interleukin-10 （IL-10）， and tumor necrosis factor-α （TNF-α） mRNA in lung tissue of the mice in various groups. Results The HE and PAS staining results showed that the mice in control group had intact airway and alveolar structure，without infiltration of inflammatory cells or mucus secretion； compared with control group， there was a large number of infiltrating inflammatory cells in airway tissue of the mice in OVA group，and the inflammation and PAS scores were increased （P<0.01）； compared with OVA group， the infiltration of inflammatory cells in airway tissue of the mice in JGYST group and OVA + JGYST group was decreased， and the inflammation and PAS scores were significantly decreased （P<0.01）. The flow cytometry results showed that compared with control group， the numbers of eosinophils， Th2 cells， and DCs in lung tissue of the mice in OVA group were increased （P<0.05 or P<0.01）， and the percentage of mature DCs and level of ROS were significantly increased （P<0.01）； compared with OVA group， the numbers of eosinophils， Th2 cells， and DCs in lung tissue of the mice in JGYST group and OVA + JGYST group were decreased （P<0.01）， and the percentage of mature DCs and level of ROS were significantly decreased （P<0.01）. The RT-qPCR results showed that compared with control group， the expression levels of IL-4， IL-10， and TNF-α mRNA in lung tissue of the mice in OVA group were increased （P<0.01）； compared with OVA group， the expression levels of IL-4 and TNF-α mRNA in lung tissue of the mice in JGYST group and OVA + JGYST group were decreased （P<0.01）， while the expression level of IL-10 mRNA was increased （P<0.01）. Conclusion JGYST can alleviate the airway tissue inflammation and mucus secretion in the mice with allergic asthma，and its mechanism may be related to reducing the number of Th2 cells and DCs， decreasing the ROS level and expression level of proinflammatory cytokine， and increasing the expression level of anti-inflammatory cytokine.

Objective To discuss the expression of programmed cell death-ligand 1 （PD-L1） in the oral squamous cell carcinoma （OSCC） cells and its effect on biological behavior of the OSCC CAL27 cells， and to clarify the possible mechanism. Methods Western blotting method was used to detect the expression levels of PD-L1 protein in the oral epithelial HOK cells and OSCC CAL27， TCA8113， and SCC15 cells； immunofluorescence staining method was used to detect the expression and localization of PD-L1 protein in the CAL27 cells. The CAL27 cells were divided into control group （transfected with si-NC） and si-PD-L1 group （transfected with si-PD-L1）. Western blotting method was used to detect the interference efficiency of the cells in two groups； CCK-8 assay was used to detect the proliferative activities of the cells in two groups at different time points； plate clone formation assay was used to detect the numbers of clone formation of the cells in two groups； cell scratch healing assay was used to detect the scratch healing rates of the cells in two groups； Transwell chamber assay was used to detect the numbers of migration and invasion cells in two groups. Results The expression level of PD-L1 protein in the OSCC cells was higher than that in the HOK cells （P<0.05 or P<0.01）； PD-L1 expressed in the cytoplasm and nucleus of the CAL27 cells. The CCK-8 assay and plate clone formation assay results showed that compared with control group， the proliferative activities of the CAL27 cells in si-PD-L1 group at different time points were significantly decreased（P<0.05 or P<0.01）， and the numbers of clone formation were significantly decreased （P<0.01）. The cell scratch healing assay results showed that compared with control group， the scratch healing rates of the cells in si-PD-L1 group were significantly decreased （P<0.05 or P<0.01）. The Transwell chamber assay results showed that compared with control group， the numbers of migration and invasion cells in si-PD-L1 group were significantly decreased （P<0.01）. Conclusion The expression of PD-L1 in the OSCC cells is higher than that in normal oral epithelial cells， and knocking down PD-L1 expression can inhibit the proliferation， clone formation， migration and invasion capabilities of the OSCC cells.

Objective To discuss the inhibitory effect of chelerythrine （CHE） on the migration， invasion， and epithelial-mesenchymal transition （EMT） of the human ovarian cancer SKOV3 cells，and to clarify the associated mechanism. Methods The SKOV3 cells were cultured in vitro and divided into control group and 2.5， 5.0， 10.0， 20.0， and 40.0 μmol·L^－1 CHE groups.Methylthiazolydiphenyl-tetrazolium（MTT） assay was used to detect the inhibitory rates of proliferation of the cells in various groups. The SKOV3 cells were cultured in vitro and divided into control group， transforming growth factor-β1 （TGF-β1） group， TGF-β1+5 μmol·L^－1 CHE group， and TGF-β1+10 μmol·L^－1 CHE group.Cell scratch assay was used to detect the migration rates of the cells in various groups； Transwell chamber assay was used to detect the numbers of migration and invasion cells in various groups； Western blotting method was used to detect the expression levels of E-cadherin， N-cadherin， and Vimentin proteins in the cells in various groups； immunofluorescence staining method was used to detect the fluorescence intensities of E-cadherin and N-cadherin in the cells in various groups. Results The MTT assay results showed that compared with control group， the inhibitory rates of proliferation of the cells in 5.0， 10.0， 20.0， and 40.0 μmol·L^－1 CHE groups were significantly increased （P<0.05 or P<0.01）. The cell scratch assay results showed that compared with control group， the migration rate of the cells in TGF-β1 group was increased （P<0.01）； compared with TGF-β1 group， the migration rates of the cells in TGF-β1+5 μmol·L^－1 CHE group and TGF-β1+10 μmol·L^－1 CHE group were significantly decreased （P<0.01）. The Transwell chamber assay results showed that compared with control group， the numbers of migration and invasion cells in TGF-β1 group were significantly increased （P<0.05）； compared with TGF-β1 group， the numbers of migration and invasion cells in TGF-β1+5 μmol·L^－1 CHE group and TGF-β1+10 μmol·L^－1 CHE group were significantly decreased （P<0.01）. The Western blotting results showed that compared with control group， the expression level of E-cadherin protein in the cells in TGF-β1 group was significantly decreased （P<0.01）， while the expression levels of N-cadherin and Vimentin proteins were increased （P<0.05 or P<0.01）； compared with TGF-β1 group， the expression levels of E-cadherin protein in the cells in TGF-β1+5 μmol·L^－1 CHE group and TGF-β1+10 μmol·L^－1 CHE group were significantly increased （P<0.01）， and the expression levels of N-cadherin and Vimentin proteins were significantly decreased （P<0.01）. The immunofluorescence staining results showed that compared with control group， the fluorescence intensity of E-cadherin in the cells in TGF-β1 group was decreased， and the fluorescence intensity of N-cadherin was increased； compared with TGF-β1 group， the fluorescence intensities of E-cadherin in the cells in TGF-β1+5 μmol·L^－1 CHE group and TGF-β1+10 μmol·L^－1 CHE group were significantly increased， and the fluorescence intensities of N-cadherin were decreased. Conclusion CHE can inhibit the proliferation， migration， invasion， and EMT of the human ovarian cancer SKOV3 cells.

Objective To discuss the differential effects of apolipoprotein E （APOE） gene polymorphism in the neurotoxicity-reactive astrocytes， and to provide the theoretical basis for the study of the pathogenesis of Alzheimer’s disease （AD）. Methods The primary cortical astrocytes from the APOE-knockout mice （APOE ^-/- ） were isolated and cultured in vitro，and the purity of the cells was identified by immunofluorescence staining. The human APOE3 and APOE4 recombinant over-expression plasmids were constructed and separately transfected into the primary APOE ^-/- astrocytes， and the APOE ^-/- primary cells were regarded as control. Western blotting method was used to detect the expression levels of APOE and glial fibrillary acidic protein （GFAP） proteins in the cells； enzyme-linked immunosorbent assay （ELISA） method was used to detect the APOE level in the cellular culture supernatant. The inflammatory models were prepared with the primary astrocytes transfected with APOE3 and APOE4 and co-stimulated with interleukin-1α（IL-1α）， tumor necrosis factor （TNF）， and complement C1q.The cells were divided into APOE3+PBS group， APOE4+PBS group， APOE3+IL-1α+TNF+C1q group， and APOE4+IL-1α+TNF+C1q group. Cell immunofluorescence staining method was used to observe the morphology of the cells in various groups； real-time fluorescence quantitative PCR （RT-qPCR） method was used to detect the expression levels of glypican 4 （Gpc4）， glypican 6 （Gpc6）， thrombospondin 1 （Thbs1）， thrombospondin 2 （Thbs2）， SPARC-like protein 1 （Sparcl1） and glial cell line derived neurotrophic factor （GDNF）， C3，and S100 calcium binding protein B （S100B） mRNA in the cells in various groups； microsphere phagocytosis assay was used to detect the phagocytic capacities of the cells in various groups； Western blotting was used to detect the protein expression levels of B-cell lymphoma 2 （Bcl-2），and cysteinyl aspartate specific protease-3 （Caspase-3） proteins in the cells in various groups. Results Compared with APOE ^-/- group， the expression levels of APOE and GFAP proteins in the cells and the APOE level in the cellular culture supernatant in transfected APOE3 and transfected APOE4 groups were increased （P<0.01）. The fluorescence microscope observation results showed that compared with APOE3+PBS and APOE4+PBS groups， the astrocytic processes in APOE3+IL-1α+TNF+Cq1 group and APOE4+IL-1α+TNF+Cq1 group became shorter and the cell bodies became larger； compared with APOE3+IL-1α+TNF+Cq1 group， the astrocytic processes in APOE4+IL-1α+TNF+Cq1 group were even shorter. Compared with APOE3+PBS and APOE4+PBS groups， the expression levels of Gpc4， Gpc6， Thbs1， Thbs2，and Sparcl1 mRNA in the cells in APOE3+IL-1α+TNF+Cq1 group and APOE4+IL-1α+TNF+Cq1 group were significantly decreased （P<0.01）； compared with APOE3+IL-1α+TNF+Cq1 group， the expression levels of Gpc4， Gpc6，Thbs1， Thbs2， and Sparcl1 mRNA in the cells in APOE4+IL-1α+TNF+Cq1 group were significantly decreased （P<0.05 or P<0.01）. Compared with APOE3+PBS and APOE4+PBS groups， the expression levels of GDNF mRNA in the cells in APOE3+IL-1α+TNF+Cq1 group and APOE4+IL-1α+TNF+Cq1 group were decreased（P<0.01），and the expression levels of C3 and S100B mRNA were increased（P<0.01）；compared with APOE3+IL-1α+TNF+Cq1 group， the expression level of GDNF mRNA in the cells in APOE4+IL-1α+TNF+Cq1 group was decreased（P<0.05），and the expression levels of C3 and S100B mRNA were increased（P<0.05）. Compared with APOE3+PBS group and APOE4+PBS group，the numbers of hagocytosis of microspheres in the cells in APOE3+IL-1α+TNF+Cq1 group and APOE4+IL-1α+TNF+Cq1 group were significantly decreased； compared with APOE3+IL-1α+TNF+Cq1 group，the number of hagocytosis of microspheres in the cells in APOE4+IL-1α+TNF+Cq1 group was significantly decreased. Compared with APOE3+PBS group and APOE4+PBS group，the expression levels of Bcl-2 protein in the cells in APOE3+IL-1α+TNF+Cq1 group and APOE4+IL-1α+TNF+Cq1 group were decreased （P<0.05 or P<0.01）and the expression levels of Caspase-3 protein were significantly increased（P<0.01）；compared with APOE3+IL-1α+TNF+Cq1 group， the expression level of Bcl-2 protein in the cells in APOE4+IL-1α+TNF+Cq1 group was decreased（P<0.01），and the expression level of Caspase-3 protein was increased（P<0.05）. Conclusion The APOE4 genotype has a stronger ability to induce the inflammatory factors compared with APOE3；it can lead to a neurotoxicity-reactive astrocyte phenotype，increase the neurotoxicity，affect the astrocyte apoptosis， and aggravate the neuron damage.

Objective To discuss the effect of ligustilide on the cardiac function and angiogenesis in the rats with heart failure，and to clarify its regulatory effect on protein kinase D1 （PKD1）/hypoxia-inducible factor-1α（HIF-1α）/vascular endothelial growth factor （VEGF） pathway. Methods The SD rats were randomly divided into sham operation group， model group， ligustilide group， PKD1/HIF-1α/VEGF signaling pathway inhibitor CID755673 （CID） group， and ligustilide+CID group. The heart failure rat model was established by ligation of the left anterior descending coronary artery. The rats in ligustilide group were injected intravenously with 20 mg·kg^－1 ligustilide， the rats in CID group were injected intraperitoneally with 50 mg·kg^－1 CID， and the rats in ligustilide+CID group were injected intraperitoneally with 50 mg·kg^－1 CID followed by intravenous injection of 20 mg·kg^－1 ligustilide， once per day for 4 consecutive weeks.The cardiac function indexes of the rats in various groups were detected by echocardiography；the percentages of myocardial infarction areas of the rats in various groups were detected by 2，3，5-triphenyltetrazolium chloride （TTC） staining； the pathomorphology of myocardium tissue of the rats in various groups was observed by HE staining； the expression levels of PKD1， HIF-1α， CD31， and VEGF mRNA and proteins in ischemic area of myocardium tissue of the rats in various groups were detected by real-time fluorescence quantitative PCR （RT-qPCR） and Western blotting methods. Results Compared with sham operation group， the rats in model group and CID group had altered myocardial cell morphology， increased intercellular gaps， disorganized arrangement， visible muscle fiber breaks and inflammatory cell infiltration； the rats in ligustilide group and ligustilide+CID group had relatively orderly myocardial fiber arrangement， fewer myocardial fiber breaks and decreased number of inflammatory cells. Compared with sham operation group， the left ventricular ejection fraction （LVEF） and left ventricular fractional shortening （LVFS） of the rats in model group were decreased （P<0.05）， the left ventricular end-systolic diameter （LVESD） and left ventricular end-diastolic diameter （LVEDD） were increased （P<0.05）， and the expression levels of PKD1， HIF-1α， CD31，and VEGF mRNA and proteins in myocardium tissue were decreased （P<0.05）. Compared with model group， the LVEF and LVFS of the rats in ligustilide group were increased （P<0.05）， the LVESD and LVEDD were decreased （P<0.05），the percentage of myocardium infarction area was decreased （P<0.05）， and the expression levels of PKD1， HIF-1α，CD31， and VEGF mRNA and proteins in myocardium tissue were increased （P<0.05）； compared with model group，the LVEF and LVFS of the rats in CID group were decreased （P<0.05）， the LVESD and LVEDD were increased （P<0.05）， the percentage of myocardium infarction area was increased （P<0.05）， and the expression levels of PKD1， HIF-1α， CD31， and VEGF mRNA and proteins in myocardium tissue were decreased （P<0.05）； compared with ligustilide group， the LVEF and LVFS of the rats in ligustilide+CID group were decreased （P<0.05）， the LVESD and LVEDD were increased （P<0.05）， the percentage of myocardium infarction area was increased （P<0.05）， and the expression levels of PKD1， HIF-1α， CD31， and VEGF mRNA and proteins in myocardium tissue were decreased （P<0.05）；compared with CID group， the LVEF and LVFS of the rats in ligustilide+CID group were increased （P<0.05）， the LVESD and LVEDD were decreased （P<0.05）， the percentage of myocardium infarction area was decreased（P<0.05）， and the expression levels of PKD1， HIF-1α， CD31， and VEGF mRNA and proteins in myocardium tissue were increased （P<0.05）. Conclusion Ligustilide can promote the angiogenesis， reduce the myocardium infarction area， and improve the cardiac function in the rats with heart failure；it works through activation of the PKD1/HIF-1α/VEGF pathway.

Objective To discuss the regulatory effect of berberine （BBR） on fatty acids in the human glioma T98G cells and its effect on the cell proliferation， migration， and invasion， and to clarify its potential mechanism. Methods The T98G cells at logarithmic growth phase were divided into control group and different concentrations （25， 50， and 100 mg·L^－1） of BBR groups. Cell wound healing assay was used to detect the migration rates of the cells in various groups； Transwell chamber assay was used to detect the invasion rates of the cells in various groups.The T98G cells at logarithmic growth phase were divided into control group and 100 mg·L^－1BBR group，and Mass spectrometry was used to detect the fatty acid contents in the cells in two groups. The T98G cells at logarithmic growth phase were divided into control group and different concentrations （50， 100， and 150 mg·L^－1） of BBR groups； Western blotting method was used to detect the expression levels of phosphatidylinositol 3-kinase （PI3K）， phosphorylated PI3K （p-PI3K）， protein kinase B （AKT）， phosphorylated AKT （p-AKT）， sterol regulatory element-binding protein 1 （SREBP-1），and fatty acid synthase （FASN） in the cells in various groups.The expression of FASN was suppressed by gene silencing technology， and the T98G cells at logarithmic growth phase were divided into control group， shFASN1 group， and shFASN2 group. Western blotting method was used to detect the expression levels of FASN protein in the cells in various groups； clone formation assay was used to detect the clone formation of the cells in various groups；cell wound healing assay was used to detect the migration rates of the cells in various groups. Results Compared with control group， the migration rates and invasion rates of the cells in different concentrations of BBR groups were decreased in a concentration-dependent manner （P<0.01）， and the fatty acid content in the cells in 100 mg·L^－1 BBR group was significantly decreased （P<0.01）.Compared with control group，the expression levels of p-PI3K，p-AKT， SREBP-1， and FASN proteins in the cells in 150 mg·L^－1 BBR group were significantly decreased （P<0.05 or P<0.01）， and the expression level of SREBP-1 protein in the cells in 100 and 150 mg·L^－1 BBR groups were significantly decreased （P<0.01）. After suppression of FASN expression， compared with control group， the expression levels of FASN protein in the cells in shFASN1 and shFASN2 groups were significantly decreased （P<0.01）， and the expression level of FASN protein in the cells in shFASN2 group was lower than that in shFASN1 group （P<0.05）； compared with control group， the numbers of clone formation and migration rates of the cells in shFASN1 and shFASN2 groups were significantly decreased （P<0.01）， and the migration rate of the cells in shFASN2 group was significantly lower than that in shFASN1 group （P<0.05）. Conclusion BBR interferes with fatty acid synthesis in the glioma T98G cells by reducing the expression of the PI3K/AKT/SREBP-1/FASN pathway related proteins， and decrease their migration and invasion capabilities.

Objective To investigate the efficacy of Balanophora involucrata Hook.f. in treatment of hyperuricemia （HUA） based on network pharmacology， molecular docking， and hyperuricemia models in vivo and in vitro，and to clarify the main targets of its active components and related signaling pathway mechanism. Methods The potential targets of Balanophora involucrata Hook.f. in treatment of HUA were identified by Databases such as the Traditional Chinese Medicine Database in Taiwan， the Chinese Herbal Medicine Identification Database，Professional Chemical Database， TargetNet Database， SwissTargetPrediction Database， GeneCards， Therapeutic Target Database （TTD），DrugBank Database， DisGeNET Database， Online Mendelian Inheritance in Man （OMIM） Database， and Venny Database. STRING Database and Cytoscape software were used to construct the active component-predictive target network and protein-protein interaction （PPI） network for Balanophora involucrata Hook.f.；topological analysis was used to select the main active components and core targets；Gene Ontology （GO） functional and Kyoto Encyclopedia of Genes and Genomes （KEGG） signaling pathway enrichment analysis were performed by R software； AutoDock Vina software was used for molecular docking validation. The NRK-52E cells were divided into blank control group， blank administration group， model group， and different concentrations （2.0， 10.0， and 50.0 μmol·L^-1） of erythrodiol （EDT） groups. High-performance liquid chromatography culture （HPLC） was used to detect the uric acid （UA） levels in the cell culture supernatants in various groups. The male ICR mice were divided into blank control group， blank administration group， model group， and EDT group； the mice in the last two groups were used to prepare the HUA models； kits were used to detect the levels of UA， creatinine （Cr）， and blood urea nitrogen （BUN） in serum of the mice in various groups；the bilateral kidney tissue of the mice was harvested and weighed； the kidney indexes of the mice in various groups were calculated；TUNEL staining was used to observe the apoptosis in kidney tissue of the mice in various groups；Western blotting method was used to detect the expression levels of protein kinase B （AKT），phosphorylated AKT （p-AKT），phosphoinositide 3-kinase （PI3K），phosphorylated PI3K（p-PI3K）， B-cell lymphoma-2 （Bcl-2）， Bcl-2-associated X protein （Bax）， and matrix metalloproteinase-9 （MMP-9） proteins in kidney tissue of the mice in various groups. Results Six active components of Balanophora involucrata Hook.f.were identified， involving 116 intersecting targets and 14 core targets.The enrichment analysis yielded 1 828 GO terms and 145 signaling pathways. The molecular docking results showed that EDT had good binding activity with MMP-9. The high uric acid cell experiment results showed that compared with blank control group， the UA level in the cells in model group was significantly increased （P<0.01）； compared with model group， the UA levels in the cells in 2.0， 10.0， and 50.0 μmol·L^-1 EDT groups were significantly decreased （P<0.01）. Compared with blank control group， the levels of UA， Cr， and BUN in serum of the mice in model group were increased（P<0.01）， and the kidney indexes were significantly increased （P<0.01）； compared with model group， the levels of UA， Cr， and BUN in serum of the mice in EDT group were decreased （P<0.05 or P<0.01），and the kidney index was significantly decreased （P<0.05 or P<0.01）. Compared with blank control group， the number of apoptotic cells in kidney tissue of the mice in model group was increased； compared with model group， the number of the apoptotic cells in kidney tissue of the mice in EDT group was significantly decreased. Compared with blank control group， the ratios of p-AKT/AKT and p-PI3K/PI3K and expression level of Bcl-2 protein in kidney tissue of the mice in model group were significantly decreased （P<0.05 or P<0.01）， while the expression levels of Bax and MMP-9 proteins were significantly increased （P<0.01）； compared with model group， the ratios of p-AKT/AKT and p-PI3K/PI3K and expression level of Bcl-2 protein in kidney tissue of the mice in EDT group were significantly increased （P<0.05 or P<0.01）， and the expression levels of Bax and MMP-9 proteins were significantly decreased （P<0.01）. Conclusion The active component of Balanophora involucrata Hook.f.，EDT，has a UA-decreasing effect and may inhibit the apoptosis and alleviate the kidney injury by activating the PI3K/AKT signaling pathway.

Objective To discuss the repairment effect of intra-articular injection of adipose derived stem cells （ADSCs） on articular cartilage destruction in the temporomandibular joint osteoarthritis （TMJOA） model rabbits， and to clarify the possible mechanism. Methods Twenty-seven rabbits were randomly divided into control group， model group， and ADSCs group. The ADSCs of the rabbits were extracted and cultured.The rabbit TMJOA model was prepared by monosodium-iodoacetate （MIA） injection technique.The temporomandibular joint cavity of the TMJOA model rabbits in ADSCs group was given two continuous intra-articular injections of 1.0×10⁶ mL^－1 ADSCs， while the rabbits in control and model group were given sequivalent volume of saline into the temporomandibular joint cavity. After 8 weeks， Micro-CT scan was performed on the temporomandibular joints of the rabbits in various groups； the bone volume fraction （BV/TV）， bone surface area/bone volume （BS/BV）， trabecular thickness （Tb.Th）， trabecular separation （Tb.Sp）， and trabecular number（Tb.N） of condyles tissue of the rabbits in various groups were analyzed； HE staining was used to observe the pathomorphology of condyles tissue of the rabbits in various groups； immunohistochemistry was used to detect the localization and expression levels of SRY-related high mobility group box gene 9（SOX9）， matrix metalloproteinase-13 （MMP-13）， and vascular endothelial growth factor （VEGF） proteins in condyles tissue of the rabbits in various groups；Western blotting method was used to detect the expression levels of SOX9， MMP-13， and VEGF proteins in condyles tissue of the rabbits in various groups. Results The micro-CT scan results showed that compared with control group， the BV/TV， Tb.Th， and Tb.N of condyles tissue of the rabbits in model group were significantly decreased （P<0.05）， while the BS/BV and Tb.Sp were significantly increased （P<0.05）； compared with model group， the BV/TV， Tb.Th， and Tb.N in condyles tissue of the rabbits in ADSCs group were significantly increased （P<0.05）， and the BS/BV and Tb.Sp were significantly decreased （P<0.05）. The HE staining results showed that the condylar cartilage surface of the rabbits in control group was smooth with clear layers and intact structure； compared with control group， the surface of condyles tissue of the rabbits in model group was irregular with thickened hypertrophic layer and areas of cell depletion and clustering； compared with model group， the pathological damage of condyles tissue of the rabbits in ADSCs group was significantly decreased.The immunohistochemical staining results showed that compared with control group and ADSCs group， the number of brown granule in condyles tissue of the rabbits in model group was increased， mainly concentrated in the hypertrophic layer，especially in the bone cartilage junction site and the expression levels of SOX9， MMP-13， and VEGF proteins in condyles tissue of the rabbits in model group were significantly increased （P<0.05）； compared with model group， the number of brown granule in condyles tissue of the rabbits in ADSCs group was significantly decreased，and the expression levels of SOX9， MMP-13， and VEGF proteins were significantly decreased（P<0.05）. The Western blotting results showed that compared with control group， the expression levels of SOX9， MMP-13， and VEGF proteins in condyles tissue of the rabbits in model group were significantly increased （P<0.05）； compared with model group， the expression levels of SOX9， MMP-13， and VEGF proteins in condyles tissue of the rabbits in ADSCs group were significantly decreased （P<0.05）. Conclusion Intra-articular injection of ADSCs can effectively repair the cartilage destruction in TMJOA， alleviate the cartilage injury， and mitigate the progression of osteoarthritis.

Objective To discuss the effect of human umbilical cord mesenchymal stem cells culture supernatant （hUCMSCs-Sup） on the proliferation， apoptosis， and endometrium receptivity of the human endometrial stromal cells （hEndoSCs） treated with mifepristone （Ms）， and to clarify the possible mechanism. Methods The hEndoSCs were cultured in vitro and divided into control group and 40， 60， 80， and 100 μmol·L^－1 Ms groups. The survival rates of the cells in various groups were detected by MTT assay. The hEndoSCs were divided into control group， 40 μmol·L^－1 Ms group， and 60 μmol·L^－1 Ms group.The apoptotic rates of the cells in various groups were detected by flow cytometry； the expression levels of apoptosis-related protein B-cell lymphoma-2 （Bcl-2） and Bcl-2-associated X protein （Bax） proteins in the cells in various groups were detected by Western blotting method， and the ratio of Bcl-2/Bax was calculated. After treated with hUCMSCs-Sup， the hEndoSCs were divided into control group， Ms group， Ms+hUCMSCs-Sup group， and Ms+hUCMSCs-Sup+3-methyladenine （3-MA） group.The survival rates of the cells in various groups were detected by MTT assay；the apoptotic rates of the cells in various groups were detected by flow cytometry；the expression levels of microtubule-associated protein 1 light chain 3B-Ⅱ （LC3B-Ⅱ） and microtubule-associated protein 1 light chain 3B-I （LC3B-Ⅰ） proteins in the cells in various groups were detected by Western blotting method， and the ratio of LC3B-Ⅱ/LC3B-Ⅰ was calculated； the expression levels of endometrium receptivity marker molecules mRNA in the cells in various groups were detected by real-time fluorescence quantitative PCR （RT-qPCR） method. Results Compared with control group， the survival rates of the cells in 40， 60， 80， and 100 μmol·L^－1 Ms groups were significantly decreased （P<0.05）in a time-dependent and dose-dependent manner. Compared with control group， the apoptotic rates of the cells in 40 and 60 μmol·L^－1 Ms groups were significantly increased （P<0.05）， and the ratios of Bcl-2/Bax were significantly decreased （P<0.05）. After treated with hUCMSCs-Sup， compared with control group， the survival rate of the cells and ratio of LC3B-Ⅱ/LC3B-Ⅰ in the cells in Ms group were significantly decreased （P<0.05）， the apoptotic rate was significantly increased （P<0.05）， and the expression levels of homeobox A10 （HOXA10）， leukemia inhibitory factor （LIF）， and integrin subunit beta 3 （ITGB3） mRNA in the cells were significantly decreased （P<0.05）；compared with Ms group， the survival rate of the cells and ratio of LC3B-Ⅱ/LC3B-Ⅰ in the cells in Ms+hUCMSCs-Sup group were significantly increased （P<0.05），the apoptotic rate was significantly decreased （P<0.05）， and the expression levels of HOXA10， LIF， and ITGB3 mRNA in the cells were significantly increased （P<0.05）； compared with Ms+hUCMSCs-Sup group， the survival rate of the cells and ratio of LC3B-Ⅱ/LC3B-Ⅰ in the cells in Ms+hUCMSCs-Sup+3-MA group were significantly decreased （P<0.05）. Conclusion hUCMSCs-Sup can increase the survival rate and decrease the apoptotic rate of the hEndoSCs after treated with Ms，and increase the endometrium receptivity，and its mechanism may be associated with the activation of autophagy of the hEndoSCs by hUCMSCs-Sup.

Objective To discuss the effect of CD40 ligand （CD40L） on the biological behavior of the human monocytic leukemia THP-1 cells through long non-coding RNA（lncRNA） linc00239，and to clarify its potential mechanism. Methods The linc00239 over-expression vector （pcDNA-linc00239） and interference vector （sh-linc00239） were constructed and transfected into the THP-1 cells.Real-time fluorescence quantitative PCR （RT-qPCR） method was used to detect the transfection efficiency. The THP-1 cells were divided into control group， vector group， pcDNA-linc00239 group， sh-linc00239 group， vector+CD40L group， pcDNA-linc00239+CD40L group， and sh-linc00239+CD40L group. RT-qPCR method was used to detect the expression levels of linc00239 in the cells in various groups； CCK-8 assay was used to detect the proliferation activities of the cells in various groups；flow cytometry was used to detect the percentages of the cells at different cell cycles and the apoptotic rates of the cells in various groups；RT-qPCR and Western blotting methods were used to to detect the expression levels of B-cell lymphoma-2 （Bcl-2） and Bcl-2-associated X protein （Bax） mRNA and proteins in the cells in various groups； Western blotting method was used to detect the expression levels of protein kinase B （AKT） and phosphorylated AKT （p-AKT） proteins in the cells in various groups，and the ratio of p-AKT/AKT was calculated. Results Compared with vector group， the proliferation activity of the cells and the percentage of the cells at G₂ phase in pcDNA-linc00239 group were significantly increased （P<0.05 or P<0.01）， the expression levels of linc00239， Bcl-2 mRNA and protein， and the ratio of p-AKT/AKT were significantly increased （P<0.05 or P<0.01），the percentage of the cells at G₁ phase， apoptotic rate， and expression levels of Bax mRNA and protein in the cells were significantly decreased （P<0.05）； compared with vector group， the proliferation activity of the cells and percentage of the cells at G₂ phase， expression levels of linc00239， Bcl-2 mRNA and protein， and ratio of p-AKT/AKT in the cells in sh-linc00239 group and vector+CD40L group were significantly decreased （P<0.05 or P<0.01）， while the percentage of the cells at G₁ phase， apoptotic rate， and the expression levels of Bax mRNA and protein in the cells were significantly increased （P<0.05 or P<0.01）；compared with pcDNA-linc00239 group， the proliferation activity of the cells and percentage of cells at G₂ phase in pcDNA-linc00239+CD40L group were significantly decreased （P<0.05 or P<0.01）， the expression levels of linc00239， Bcl-2 mRNA and protein，and ratio of p-AKT/AKT were significantly decreased （P<0.05 or P<0.01），while the percentage of cells at G₁ phase， apoptotic rate， and the expression levels of Bax mRNA and protein were significantly increased （P<0.05 or P<0.01）；compared with sh-linc00239 group， the proliferation activity of the cells and percentage of cells at G₂ phase in sh-linc00239+CD40L group were significantly decreased （P<0.05 or P<0.01）， the expression levels of linc00239， Bcl-2 mRNA and protein， and ratio of p-AKT/AKT were significantly decreased （P<0.05 or P<0.01），and the percentage of the cells at G₁ phase， apoptotic rate， and expression levels of Bax mRNA and protein were significantly increased （P<0.05 or P<0.01）. Conclusion CD40L can inhibit the proliferation and cell cycle progression of the THP-1 cells through linc00239 and induce the apoptosis.

Objective To discuss the protective effect of gingerone on the hippocampal neuron HT22 cells after oxygen-glucose deprivation/reoxygenation （OGD/R），and to clarify the related mechanism. Methods The HT22 cells were cultured， and the OGD/R cell injury model was established by setting the gradient of OGD/R time. The HT22 cells were divided into control group，OGD/R group， OGD/R+1 μmol·L^－1 gingerone group， OGD/R + 10 μmol·L^－1 gingerone group， OGD/R+100 μmol·L^－1 gingerone group，and OGD/R+0.2% dimethyl sulfoxide（DMSO） group.The viability of the cells in various groups was detected by CCK-8 assay； the survival rates of the cells in various groups were calculated to determine the optimal drug concentration of gingerone. The cells were divided into control， OGD/R group， OGD/R+ gingerone， and OGD/R+gingerone+nuclear factor erythroid-2-related factor 2（Nrf2） inhibitor（ML385） groups.The cells in OGD/R + gingerone group were treated with gingerone for 4 h before OGD treatment for 8 h followed by reoxygenation for 8 h， and the cells in OGD/R+gingerone+ML385 group were treated with 10 μmol·L^－1 ML385 for 6 h before gingerone treatment. The viability of the cells in various groups was detected by CCK-8 assay；the expression levels of Nrf2， heme oxygenase-1 （HO-1）， B-cell lymphoma-2 （Bcl-2）， and Bcl-2-associated X protein （Bax） proteins in the cells in various groups were detected by Western blotting method；the activity of superoxide dismutase （SOD） and the level of malondialdehyde （MDA） in the cell culture supernatant in various groups were detected by enzyme-linked immunosorbent assay （ELISA） method. Results Compared with control group， the survival rate of the HT22 cells was below 50% after treated with OGD for 8 h and reoxygenation for 8 h， so the HT22 cell OGD/R model was established by treated with OGD for 8 h and reoxygenation for 8 h. Compared with OGD/R group，the survival rates of the cells in OGD/R+different doses of gingerone groups were increased to various extents， and the survival rate of the cells in OGD/R+ 100 μmol·L^－1 gingerone group was significantly increased （P<0.01）； so 100 μmol·L^－1 gingerone was used for the subsequent experiment. Compared with control group， the viability of the cells in OGD/R group was significantly decreased （P<0.01）， and the expression levels of Nrf2， HO-1， and Bax proteins in the cells were significantly increased （P<0.01）， while the expression level of Bcl-2 protein in the cells was significantly decreased （P<0.05）， and the SOD activity in the cell culture supernatant was significantly decreased （P<0.01）， and the level of MDA was significantly increased （P<0.01）； compared with OGD/R group， the viability of the cells in OGD/R + gingerone group was significantly increased （P<0.01）， and the expression levels of Nrf2， HO-1， and Bcl-2 proteins in the cells were significantly increased （P<0.05 or P<0.01）， while the expression level of Bax protein in the cells was decreased（P<0.05）， the SOD activity in the cell culture supernatant was significantly increased （P<0.01）， and the level of MDA was significantly decreased （P<0.01）； compared with OGD/R + gingerone group， the viability of the cells in OGD/R + gingerone + ML385 group was significantly decreased （P<0.01）， and the expression levels of Nrf2， HO-1， and Bcl-2 proteins were significantly decreased （P<0.01）， while the expression level of Bax protein in the cells was significantly increased （P<0.01），the SOD activity in the cell culture supernatant was significantly decreased （P<0.01）， and the level of MDA was significantly increased （P<0.05）. Conclusion Gingerone alleviates the oxidative stress damage，and thereby plays an inhibiory effect on the apoptosis of the HT22 neurons by activating the Nrf2/HO-1 signaling pathway after OGD/R.

objective To prepare a composite photocrosslinked hydrogel containing zeolite imidazole framework-8 （ZIF-8），and to evaluate its in vitro cytotoxicity， drug release capability， and antimicrobial propertie. Methods The ZIF-8 particles were synthesized by hydrothermal method， and the microstructure characteristic was observed under scanning electron microscope （SEM）. The particles were mixed with the gelatin methacryloyl （GelMA） with the mass fraction of 0.2% to obtain the composite hydrogel GelMA-Z. The atomic absorption spectroscope was used to detect the cumulative zinc ion （Zn²⁺） release amounts in GelMA-Z at different time points.The NIH-3T3 cells were co-cultured with GelMA-Z for 1， 3， and 7 d；the viabilities of the cells in various groups were detected by CCK-8 assay； the GelMA-Z was co-cultured with Escherichia coli （E. coli） and Staphylococcus aureus （S. aureus） for 6，12，and 24 h and divided into control group， GelMA group， and GelMA-Z group.The bacterial activities of the cells in various groups at different time points were detected by microplate reader； the bacterial formation and the presence of live/dead becterial staining condition were detected by plate antibacterial experiment and live/dead bacterial staining method. Results The SEM observation results showed that the hydrothermally synthesized ZIF-8 particles had the uniform particle sizes.The atomic absorption spectroscope results showed that Zn²⁺ in GelMA-Z showed an initial burst phase within 1 d， followed by a slow release，and reached the equilibrium around 7 d.Compared with control group，the viabilities the cells in GelMA group and GelMA-Z group were above 90% on the 1st， 3rd， and 7th days， but there was no significant difference（P>0.05）.The bacterial activity detection results showed that when co-cultured with bacteria for 6，12，and 24 h， compared with control group and GelMA group，the bacterial activities of the E. coli and S. aureus in GelMA-Z group were decreased （P<0.05）. The plate antibacterial experiment results showed that the number of bacterial formation in GelMA-Z group was fewer than those in control group and GelMA group. The live/dead bacterial staining results showed that in GelMA-Z group，there was a large number of red fluorescence stained dead bacteria； in control group and GelMA group， there was a large number of green fluorescence stained live bacteria. Conclusion The GelMA hydrogel loaded with ZIF-8 particles can achieve the in situ photocrosslinking and possesses good Zn²⁺ release capability and antimicrobial activity， and it is a novel hydrogel dressing for treatment of the infected wounds.

Objective To discuss the effect of downregulating the proline-rich protein 11 （PRR11） expression on drug resistance of the esophageal cancer drug resistant cells， and to clarify the related mechanism. Methods The drug resistant cells EC9706/cisplatin（DDP） were established by incrementally stimulating the human esophageal cancer EC9706 cells with the increasing concentrations of DDP. The drug sensitivity of the EC9706/DDP cells was detected by MTT assay； the expression levels of PRR11 mRNA and protein in the EC9706/DDP cells and their parent EC9706 cells were detected by real-time fluorescence quantitative PCR （RT-qPCR） and Western blotting methods. The EC9706/DDP cells were divided into control group，sh-NC group （infected with sh-NC），sh-PRR11 group（infected with sh-PRR11）， sh-NC+DDP group （infected with sh-NC and treated with 4 mg·L^－1 DDP）， and sh-PRR11+DDP group （infected with sh-PRR11 and treated with 4 mg·L^－1 DDP）. The expression levels of PRR11 mRNA in the cells in various groups were detected by RT-qPCR method； the expression levels of PRR11， phosphoinositide 3-kinase （PI3K） p110α， protein kinase B （AKT）， phosphorylated AKT （p-AKT）， P-glycoprotein （P-gp）， and multidrug resistance-associated protein 1 （MRP1） proteins in the cells in various groups were detected by Western blotting method；the apoptotic rates of the cells in various groups were detected by flow cytometry. Results The DDP-resistant cell line EC9706/DDP was successfully obtained，and the drug resistance index was 7.23±0.86. Compared with the EC9706 cells， the expression levels of PRR11 mRNA and protein in the EC9706/DDP cells were increased （P<0.05）. Compared with control and sh-NC groups， the expression levels of PRR11 mRNA and protein in the cells in sh-PRR11 group were decreased （P<0.05），and the 50% inhibitory concentration （IC₅₀） of DDP was decreased （P<0.05）.Compared with sh-NC group，the expression levels of PI3K p110α， p-AKT， P-gp， and MRP1 proteins in the cells in sh-NC+DDP and sh-PRR11 groups were decreased （P<0.05），and the apoptotic rate of the cells was increased （P<0.05）. Compared with sh-NC+DDP group and sh-PRR11 group，the expression levels of PI3K p110α， p-AKT， P-gp， and MRP1 proteins in the cells in sh-PRR11+DDP group were increased（P<0.05），and the apoptotic rate of the cells was increased（P<0.05）. Conclusion Downregulating the expression of PRR11 gene in the drug resistant EC9706/DDP cells can inhibit the expressions of drug resistance-related proteins， reverse the resistance to DDP， and induce the apoptosis； its mechanism may be related to the inhibition of activation of the PI3K/AKT signaling pathway.

Objective To discuss the protective effect of velvet antler peptide （VAP） in the osteoporosis （OP） model rats，and to clarify the possible mechanism. Methods Sixty 12-week-old SD rats were randomly divided into control group， model group， positive drug group （treated with 1 mg·kg^－1·d^－1 of alendronate sodium by gavage）， low dose of VAP group （treated with 100 mg·kg^－1·d^－1 VAP), medium dose of VAP group （treated with 200 mg·kg^－1·d^－1 VAP), and high dose of VAP group （treated with 300 mg·kg^－1·d^－1 VAP), and there were ten rats in each group. Except for control group，the rats in the other groups were injected with dexamethasone （2 mg·kg^－1) to replicate the OP rat model， while the rats in control group were injected with the equivalent volume of saline twice a week for 11 consecutive weeks. Dual-energy X-ray absorptiometry was used to detect the bone mineral density （BMD） of femur tissue of the rats in various groups；enzyme-linked immunosorbent assay （ELISA） method was used to detect the levels of serum calcium （Ca²⁺）， phosphate （P）， osteoprotegerin （OPG）， alkaline phosphatase （ALP）， and osteocalcin （OCN）in serum of the rats in various groups； biochemical method was used to detect the malondialdehyde （MDA） level and superoxide dismutase （SOD） activity in serum of the rats in various groups； HE staining was used to observe the pathomorphology of bone tissue of the rats in various groups； Western blotting method was used to detect the expression levels of silent information regulator 1 （SIRT1）， catalase （CAT）， Runt-related transcription factor 2 （RUNX2）， and forkhead box protein O1 （FOXO1） proteins in bone tissue of the rats in various groups. Results Compared with control group， the BMD of femoral tissue of the rats in model group was decreased （P<0.05）； compared with model group， the BMD of femur tissue of the rats in positive drug group， medium dose of VAP group， and high dose of VAP group were increased （P<0.05 or P<0.01）. Compared with control group， the levels of Ca²⁺， P， OPG， and SOD activities in serum of the rats in model group were decreased （P<0.05）， and the levels of ALP， OCN， and MDA were increased （P<0.05）； compared with model group， the level of OPG in serum of the rats in low dose of VAP group was significantly increased（P<0.05），the levels of Ca²⁺， P， OPG， and activities of SOD in serum of the rats in positive drug group， medium dose of VAP group， and high dose of VAP group were significantly increased （P<0.05 or P<0.01）， and the levels of ALP， OCN， and MDA in serum of the rats in positive drug group and different doses of VAP groups were decreased （P<0.05 or P<0.01）. The HE staining results showed that compared with control group， the rats in model group had fewer bone cells and disordered arrangements in the bone tissue， thinner bone trabeculae with large fractures， and an expanded marrow cavity； compared with model group， the rats in positive drug group， medium dose of VAP group， and high dose of VAP group had thicker bone trabeculae arranged more tightly. The Western blotting results showed that compared with control group， the expression levels of SIRT1， CAT， RUNX2， and FOXO1 proteins in bone tissue of the rats in model group were decreased （P<0.05）； compared with model group， the expression levels of SIRT1， CAT， RUNX2， and FOXO1 proteins in bone tissue of the rats in positive drug group， medium dose of VAP group， and high dose of VAP group were significantly increased （P<0.05 or P<0.01）. Conclusion VAP has the protective effect against OP in the rats， and its mechanism may be related to mediating the antioxidant stress action through the SIRT1/FOXO1 signaling pathway.

Objective To discuss the effect of apolipoprotein C1 （APOC1） expression on the proliferation and apoptosis of the hepatocellular carcinoma cells， and to preliminarily clarify the related molecular mechanism. Methods The expression level of APOC1 mRNA in hepatocellular carcinoma tissue and its relationship with the prognosis of the patient were analyzed by The Cancer Genome Atlas （TCGA） Database； real-time fluorescence quantitative PCR （RT-qPCR） method was used to detect the expression levels of APOC1 mRNA in different hepatocellular carcinoma cells； the human liver cancer HepG2 cells with low APOC1 expression were selected as the subjects. The HepG2 cells were transfected with pcDNA3.1-APOC1 plasmid to over-express APOC1 （APOC1 over-expression group），and the HepG2 cells transfected with empty vector pcDNA3.1 were regarded as control group. MTS assay and 5-ethynyl-2'-deoxyuridine （EdU） staining were used to detect the proliferative activities and proliferation rates of the cells in two groups； Transwell chamber assay was used to detect the numbers of migration cells in two groups；flow cytometry and TUNEL assay were used to detect the percentages of the cells at different cell cycles and apoptotic rates in two groups；Western blotting method was used to detect the expression levels of extracellular regulated protein kinase （ERK）， phosphorylated ERK （p-ERK）， protein kinase B （AKT）， phosphorylated AKT （p-AKT）， B-cell lymphoma-2 （Bcl-2）， and cleaved cysteinyl aspartate specific proteinase-3（cleaved caspase-3） proteins in the cells in two groups. Results The TCGA Database results showed that the expression level of APOC1 mRNA in hepatocellular carcinoma tissue was lower than that in normal liver tissue （P<0.05）， and the patients with low expression of APOC1 mRNA had poor prognosis. The RT-qPCR results showed that the expression level of APOC1 mRNA in the HepG2 cells was the lowest， and the HepG2 cells were chosen for the subsequent research. Compared with control group， the proliferative activity and proliferation rate of the cells in APOC1 over-expression group were decreased （P<0.05 or P<0.01），the number of migration cells was decreased （P<0.01），and the percentage of the cells at S phase and the apoptotic rate were significantly increased （P<0.01）. Compared with control group， the expression levels of p-ERK， p-AKT， and Bcl-2 proteins in the cells in APOC1 over-expression group were significantly decreased （P<0.05），and the expression level of cleaved caspase-3 protein was increased （P<0.01）. Conclusion High expression of APOC1 can inhibit the proliferation of the human liver cancer HepG2 cells and induce the apoptosis，and its mechanism may be related to inhibition of the expressions of p-ERK，p-AKT，Bcl-2 proteins and promotion of the expression of cleaved caspase-3 protein.

Objective To discuss the improvement effect of curcumin combined with fecal bacteria transplantation on the mice with dextran sulfate sodium （DSS）-induced ulcerative colitis （UC），and to clarify the related mechanism. Methods Fifty mice were randomly divided into control， model， curcumin， fecal bacteria transplantation， and combination groups. Except for the mice in control group （given distilled water），the mice in the other groups were given distilled water containing 2% DSS to establish the UC models. The mice in curcumin group were gavaged with 0.4 mL of 60 mg·kg^－1 curcumin solution once per day for 10 d； the mice in fecal bacteria transplantation group underwent enema with 0.2 mL of fecal bacteria suspension once per day for 10 d； the mice in combination group received the enema of 0.2 mL fecal bacteria suspension and gavaged with 0.4 mL of 60 mg·kg^－1 curcumin solution. At the end of the experiment， the disease activity index （DAI） and colon macroscopic damage index （CDMI） of the mice in various groups were calculated； the morphology of colon tissue of the mice in various groups was detected by HE staining；the levels of interleukin （IL）-1β， tumor necrosis factor-α（TNF-α）， IL-4， and IL-10 in colon tissue of the mice in various groups were detected by enzyme-linked immunosorbent assay （ELISA） method；the expression levels of occludin and zonula occludens-1 （ZO-1） mRNA and proteins in colon tissue of the mice in various groups were detected by real-time fluorescence quantitative（RT-qPCR） and Western blotting methods. Results The intestinal mucosal epithelial structure of the mice in control group was intact and continuous with regular glandular arrangement and without inflammatory cell infiltration or ulceration； the intestinal mucosal epithelial structure of the mice in model group exhibited loss of colonic mucosal epithelium， disordered glandular arrangement， reduced goblet cells， congestion and edema in mucosal and submucosal layers， and extensive infiltration of inflammatory cells with widespread small ulcers； the intestinal mucosal epithelial structure of the mice in curcumin， fecal bacteria transplantation， and combination groups exhibited relatively intact colonic mucosal epithelial structures with reduced inflammatory cell infiltration and ameliorated mucosal and submucosal congestion and edema. Compared with control group， the DAI and CDMI of the mice in model group were increased （P<0.05）， the levels of IL-1β and TNF-α were increased （P<0.05）， the levels of IL-4 and IL-10 were decreased （P<0.05），and the expression levels of occludin and ZO-1 mRNA and proteins were decreased （P<0.05）；compared with model group， the DAI and CDMI of the mice in curcumin， fecal bacteria transplantation， and combination groups were decreased （P<0.05），the levels of IL-1β and TNF-α were decreased （P<0.05）， the levels of IL-4 and IL-10 were increased （P<0.05）， and the expression levels of occludin and ZO-1 mRNA and proteins were increased （P<0.05）. Compared with curcumin group and fecal bacteria transplantation group，the DAI and CDMI of the mice in combination group were decreased （P<0.05），the levels of IL-1β and TNF-α were decreased （P<0.05）， the levels of IL-4 and IL-10 were increased （P<0.05）， and the expression levels of occludin and ZO-1 mRNA and proteins were increased （P<0.05）. Conclusion Curcumin combined with fecal bacteria transplantation can ameliorate the pathological damage in colonic tissue of the UC mice， inhibit the secretion of inflammatory factors， and promote the repaiment of intestin mucosa.

Objective To discuss the effect of downregulating of high mobility group box protein 2 （HMGB2） expression on the biological behavior of the liver cancer cells and the epithelial-mesenchymal transition （EMT） process， and to clarify its mechanism. Methods The human liver cancer LM3 cells at logarithmic growth phase were divided into negative control group and HMGB2 RNA interference group （HMGB2 siRNA group）；the cells in two groups were transfected with RNA oligonucleotides（RNA oligos） with irrelevant sequences and RNA oligos designed to knock down HMGB2， and the Lipofectamine 2000 was regarded as the vector.The expression levels of HMGB2 mRNA and protein in the cells in two groups were detected by real-time fluorescence quantitative PCR （RT-qPCR） and Western blotting methods； cell scratch assay and Transwell chamber assay were used to detect the migration and invasion abilities of the cells in two groups； the expression levels of E-cadherin， N-cadherin， and Vimentin proteins and protein kinase B （AKT）/mammalian target of rapamycin （mTOR） pathway related proteins in the cells in two groups were detected by Western blotting method. Results Compared with negative control group， the expression levels of HMGB2 mRNA and protein in the cells in HMGB2 siRNA group were significantly decreased （P<0.05），the cell scratch healing rate was significantly decreased （P<0.01），the number of invasion cells was significantly decreased （P<0.01），and the expression level of E-cadherin protein in the cells was significantly increased （P<0.01）， while the expression levels of N-cadherin， Vimentin， mTOR， AKT， and phosphorylated AKT （p-AKT） proteins in the cells were significantly decreased （P<0.05 or P<0.01）. Conclusion Downregulating the expression of HMGB2 can reduce the migration and invasion abilities of the liver cancer LM3 cells and inhibit the EMT，and its mechanism may be related to regulating the expression of the AKT/mTOR pathway related proteins.

Objective To discuss the effect of royal jelly acid （10-HDA） on the proliferation and migration of the human colon cancer SW620 cells based on the network pharmacology， and to clarify its related molecular mechanism. Methods The active ingredients such as 10-HDA and their corresponding targets were retrieved by using the keyword “royal jelly” from the Traditiomal Chinese Medicine Systems Pharmacology （TMSCP）Database and the Traditiomal Chinese Medicine Integrated Database （TCMID）； the small molecule targets were predicted by the Swiss Target Prediction Database.The GeneCards Database and the Online Mendelian Inheritance in Man（OMIM） Database were used to obtain the targets with the keyword “Colon Cancer”；the protein-protein interaction （PPI） network was constructed by using the String Database and Cytoscape 3.8.0 Software to screen the core targets； the Gene Ontology （GO） function enrichment analysis and Kyoto Encyclopedia of Genes and Genomes （KEGG） signaling pathway enrichment analysis were analyzed by Metascape Database； the specific ingredient 10-HDA was screened for the in vitro activity experiments. The human colon cancer SW620 cells with good growth status were divided into control group and different doses （1， 5， 10， 15， and 20 mmol·L^－1） of 10-HDA groups. The viabilities of the cells in various groups were detected by MTT method and the survival rates of the cells were calculated. The SW620 cells were divided into control group， low dose （5 mmol·L^－1） of 10-HDA group， middle dose （10 mmol·L^－1） of 10-HDA group， and high dose （15 mmol·L^－1） of 10-HDA group； Hoechst33342 staining method was used to observe the morphology of the cells in various groups； cell scratch test was used to detect the scratch healing rates of the cells in various groups；flow cytometry was used to detect the percentages of the cells at different cell cycles in various groups； biochemical method was used to detect the activities of total antioxidant capacity （T-AOC） and superoxide dismutase （SOD） in the cells in various groups； Western blotting method was used to detect the expression levels of B-cell lymphoma 2 （Bcl-2）， Bcl-2-associated X protein （Bax），cysteine-containing aspartate proteolytic enzyme-3 （Caspase-3）， cysteine-containing aspartate proteolytic enzyme-9 （Caspase-9）， glycogen synthase kinase 3β （GSK3β）， β-catenin， and cyclin D1 proteins in the cells in various groups. Results Six active ingredients of royal jelly were screened out by the TCMSP Database， and 28 core targets of 10-HDA in the treatment of colon cancer were obtained. The GO function enrichment analysis mainly included the signaling pathways such as cell proliferation and apoptosis. The KEGG signaling pathway enrichment analysis included the cell cycle， prostate cancer， cell senescence， and p53 signaling pathways； the GSK3β/β-catenin signaling pathway was closely related to the cell cycle. Compared with control group， the viabilities of the cells in 5，10，15， and 20 mmol·L^－110-HDA groups were decreased in a dose-dependent manner （P<0.05 or P<0.01）， the numbers of apoptotic cells in different doses of 10-HDA groups were significantly increased， and the scratch healing rates of the cells were significantly decreased （P<0.05 or P<0.01）； the percentages of the cells at S phase in middle and high doses of 10-HDA groups were significantly increased （P<0.05 or P<0.01），the activities of T-AOC and SOD in the cells in different doses of 10-HDA groups were significantly decreased （P<0.05 or P<0.01）. Compared with control group， the expression level of Bcl-2 protein in the cells in low dose of 10-HDA group was significantly decreased （P<0.01）， and the expression level of GSK3β protein was significantly increased （P<0.05）； compared with control group， the expression levels of Bax， Caspase-3， Caspase-9， and GSK3β proteins in the cells in middle and high doses of 10-HDA groups were significantly increased （P<0.05 or P<0.01）， and the expression levels of Bcl-2， β-catenin，and CyclinD1 proteins were significantly decreased （P<0.01）. Conclusion 10-HDA can significantly inhibit the proliferation and migration of the colon cancer cells and promote the apoptosis and oxidation levels of the colon cancer cells，and its mechanism may be related to the activation of the GSK3β / β-catenin signaling pathway.

Objective To analyze the improvement effect of monk fruit on diabetic nephropathy（DN） by network pharmacology，and to elucidate its possible related mechanism. Methods The Traditional Chinese Medicine Systems Pharmacology（TCMSP） Database was used to detect the active ingredients and their targets of monk fruit； the DN target genes were screened out by DisGeNET Database and Genecards Database； the key targets of monk fruit against DN were obtained by comparing the monk fruit with DN targets； protein-protein interaction （PPI） network diagram was constructed by STRING Database and Cytoscape software； Gene Ontology （GO） functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes （KEGG） signaling pathway enrichment analysis were performed by Cytoscape software.Molecular docking technology was used to predict the binding abilities of the core targets and the main active ingredients of monk fruit. Results The TCMSP Database combined with the selection criteria was used to screen out a total of five active ingredients of monk fruit （ZINC03860434， Perlolyrine， beta-sitosterol， Kaempferol， and Flazin） as well as 85 targets represented by serine/threonine protein kinase 1 （AKT1），transcription factor RELA， c-Jun N-terminal kinase （JUN），and tumor necrosis factor （TNF）. Among them， Kaempferol contained the most targets.Among the 85 targets， 34 were associated with DN.The GO functional enrichment analysis mainly included biological process（BP） such as oxidative stress， regulation of inflammation and apoptosis， and cell signaling transduction.The KEGG enrichment analysis included advanced glycosylation end product（AGE）-receptor of AGE （AGE-RAGE） signaling pathway， TNF signaling pathway， and C-type lectin receptor signaling pathway.The results molecular docking technology of the main active ingredients of monk fruit and DN target proteins showed that 5 kinds of molecular docking engergy were －8.00－－5.00 kJ·mol^－1. Conclusion Kaempferol is the most effective active ingredient in the monk fruit for the treatment of DN， and its mechanism is mainly related to anti-inflammatory.

Objective To screen the interacting protein of ubiquitin-conjugating enzyme E2S （UBE2S） and construct the hepatocellular carcinoma （HCC） based on UBE2S interacting protein prognosis model （UIPM），and to discuss the value of UIPM in assessing the prognosis of the HCC patients. Methods Co-immunoprecipitation （Co-IP） was used to screen the protein complexes binding to Flag-UBE2S. After validation by sodium dodecyl sulphate-polyacrylamide gel electrophoresis （SDS-PAGE） and Western blotting methods；liquid chromatography-mass spectrometer （LC-MS） was used to identify the UBE2S interacting proteins； Gene Ontology （GO） functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes （KEGG） signaling pathway enrichment analysis were conducted on these proteins； the prognosis-related proteins from The Cancer Genome Atlas （TCGA） were cross-referenced with UBE2S interacting proteins by survival package of R software；the key proteins were extracted through LASSO regression analysis to build the UIPM； the prognostic model risk scoring formula was established. The HCC patients in TCGA were divided into high risk group and low risk group based on median value of the risk scores. The predictive accuracy of UIPM was evaluated by receiver operating characteristic curve （ROC）， and the predictive accuracy was further validated by International Cancer Genome Consortium （ICGC） Database； univariate regression analysis and multivariate Cox regression analysis were used to detect whether the UIPM risk score was an independent prognostic factor for HCC. Furthermore， the nomogram model was built. Results A total of 97 UBE2S interacting proteins were identified through Co-IP combined with LC-MS analysis.The GO functional enrichment analysis and KEGG signaling pathway enrichment analysis results showed that the interacting proteins were closely associated with cysteine-type endopeptidase activity， oxidative stress， and cell death. The TCGA revealed 5 163 HCC prognosis-related proteins； after intersecting with UBE2S interacting proteins， 40 prognosis-related interacting proteins were found. Seven key proteins were determined through LASSO regression analysis， including UBE2S， heat shock protein family A member 8 （HSPA8）， heterogeneous nuclear ribonucleoprotein H1 （HNRNPH1），chaperonin containing TCP1 subunit 3 （CCT3），eukaryotic translation initiation factor 2 subunit 1 （EIF2S1）， receptor for activated C kinase 1 （RACK1）， and actin related protein 2/3 complex subunit 4 （ARPC4）， and the UIPM was constructed. There was significant difference in survival rate of the patients between high risk group and low risk group （P<0.05）. The ROC curve analysis results showed the area under ROC curve（AUC） values of UIPM for predicting 1-year， 2-year， and 3-year survival risk scores of the HCC patients were all greater than 0.7， indicating the model had high predictive accuracy. This was also confirmed by ICGC Database data. The univariate and multivariate Cox regression analysis results showed that the UIPM risk score was an independent prognostic risk factor for the HCC patients （P<0.05）. The nomogram results showed good consistency between predicted survival rate and actual survival rate of the patient. Conclusion A total of 97 interacting proteins that interact with UBE2S may promote the occurence and devolopment of HCC through oxidative stress and dysregulation of ferroptosis pathways. The UIPM risk score is an independent risk factor for the prognosis of HCC and can be used to predict the outcomes of the patients. UBE2S， HSPA8， HNRNPH1， CCT3， EIF2S1， RACK1， and ARPC4 could be regarded as the new biomarkers and therapeutic targets for HCC.

Objective To screen the aging genes closely associated with pelvic organ prolapse （POP） by bioinformatics techniques， and to clarify the potential clinical significance and value of key genes. Methods Gene Expression Omnibus （GEO） Database was used to download the datasets GSE53868 and GSE151188 for POP-related genes with the keyword “pelvic organ prolapse”. The aging-related genes were obtained from Aging Atlas， CellAge， and the Human Ageing Genomic Resources （HAGR） Databases；the intersection of genes related with POP in two groups provided a list of differentially expressed genes （DEGs） associated with aging in POP； gene Set Enrichment Analysis （GSEA） was conducted with R software version 4.2.1； Gene Ontology （GO） functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes （KEGG） signaling pathway enrichment analysis of DEGs were conducted by the Database for Annotation， Visualization and Integrated Discovery （DAVID）； the protein-protein interaction （PPI） network was constructed with Cytoscape 3.9.1 software；the top 10 Hub genes were selected by cytoHubba plugin； the infiltration of 22 types of immune cells in the patients in POP group and control group was analyzed by CIBERSORT deconvolution method using R software；the key genes were further screened by LASSO regression algorithm； the correlation and diagnostic efficacy between key genes and immune cell infiltration were analyzed. Results From the Aging Atlas， CellAge， and HAGR Databases， 724 aging-related genes were identified. Intersection with the POP expression profile yielded an aging gene expression matrix related to POP containing 624 genes， and 29 POP-related DEGs were identified after differential analysis， including 2 upregulated genes and 27 downregulated genes. The GSEA results showed that the upregulated pathways were mainly related to diabetes and cellular senescence， whereas the downregulated pathways included Alzheimer’s disease and hypoxia-inducible factor-1 （HIF-1） signaling pathways.The GO functional enrichment analysis mainly enriched in the biological processes such as the response of the cells to lipopolysaccharide， inflammatory response， and negative regulation of cell proliferation. The KEGG signaling pathway enrichment analysis mainly enriched in interleukin-17 （IL-17）， tumor necrosis factor （TNF）， and nuclear factor-kappa B （NF-κB） signaling pathways. The PPI network analysis got 10 Hub genes including interleukin-6 （IL-6）， interleukin-1B （IL-1B）， prostaglandin-endoperoxide synthase 2 （PTGS2）， and NF-kappa-B inhibitor alpha （NFKBIA）. The CIBERSORT deconvolution method results showed a relatively higher infiltration proportion of neutrophils and activated mast cells in the patients in POP group， the activated mast cells had a positive correlation with most of the DEGs （r>0.5） and the macrophages had a significant positive correlation with IL-1B （r>0.6）. The key genes Jun D proto-oncogene （JUND）， Snail homolog 1 （SNAI1）， amphiregulin （AREG）， Lamin A/C （LMNA）， and superoxide dismutase 2 （SOD2） selected by LASSO regression analysis had high diagnostic efficacies， and the area under receiver operating characteristic curve （ROC） （AUC） were all greater than 0.75. Conclusion During the aging process，the genes such as JUND，SNAI1，AREG，LMNA，and SOD2 may participate in the pathophysiology of POP through various pathways，including inflammation-related pathways，transcription regulation，and affecting collagen secretion and metabolism，thereby influence the connective tissue support function and promote the occurrence and development of POP.

Objective To discuss the factors related to the prognosis in the alpha fetoprotein （AFP） negative hepatocellular carcinoma （HCC） patients，and to construct the nomogram for predicting the survival time of the patients. Methods The retrospective analysis on data of 2 064 cases of AFP negative HCC patients extracted from the Surveillance， Epidemiology， and End Results （SEER） Database was conducted， and all the patients were divided into training cohort and internal validation cohort at a ratio of 7∶3， and 101 AFP negative HCC patients from the Integrated Traditional Chinese and Western Medicine Hospital in Hunan Province were regarded as the external validation cohort.The univariate Cox regression analysis results were incorporated into the multivariate analysis， and the independent risk factors for the AFP negative HCC patients were obtained by multivariate Cox analysis to build a cancer specific survival （CSS） prognosis nomogram for the AFP negative HCC patients. The predictive efficacy and clinical utility of the nomogram were evaluated by time-dependent receiver operating characteristic curve （ROC）， calibration plots， and decision curve analysis （DCA）. The total score obtained from the nomogram was used for the risk stratification to compare the degree of risk discrimination between the nomogram and the American Joint Committee on Cancer （AJCC） staging system. Results Ten independent risk factors were selected by multivariate Cox regression analysis to construct 3-year， 4-year， and 5-year CSS prognostic nomograms for the AFP negative HCC patients， including the patient’s age， pathological grade， surgical status， radiotherapy status， chemotherapy status， lung metastasis status， tumor size， tumor T stage， tumor M stage， and marital status. The area under curve （AUC） for the 3-year， 4-year， and 5-year time-dependent ROC in the training cohort were 0.807 （95% CI： 0.786－0.828）， 0.804 （95% CI： 0.782－0.826）， and 0.813 （95% CI： 0.790－0.835）， respectively. In the internal validation cohort， they were 0.776 （95% CI： 0.743－0.810）， 0.772 （95% CI： 0.737－0.808）， and 0.789 （95% CI： 0.752－0.826）， and in the external validation cohort， they were 0.773 （95% CI： 0.677－0.868）， 0.746 （95% CI： 0.620－0.872）， and 0.736 （95% CI： 0.577－0.895）. The calibration plots verified that the nomogram fitted well with the perfect line.The DCA curve revealed that the net benefit of the nomogram was significatly higer than that of the AJCC staging system at certain probability thresholds compared with AJCC staging， the nomogram had a better ability to identify high-risk individuals. Conclusion The serum AFP expression is one of the prognostic markers for the HCC patients. For those patients with AFP negative expression in serum， different considerations should be taken. The nomogram model based on multiple risk factors is a promising clinical tool for assessing the CSS in the AFP negative HCC patients.

Objective To select the differential prognostic lactic acid metabolism-related genes （LRGs） of the head and neck squamous cell carcinoma （HNSCC） to construct the LRGs prognostic model of HNSCC， and to clarify the potential mechanism. Methods The HNSCC gene expression and clinical data were obtained from The Cancer Genome Atlas （TCGA） and Gene Expression Omnibus （GEO） Databases， the LRGs were identified through GeneCards Database， and R software was used to screen out the LRGs of HNSCC； univariate Cox regression analysis was used to identify prognosis-related genes； two different subtypes were identified based on the prognostis-related LRGs； Kaplan-Meier （K-M） curve analysis was used to compare the prognosis of the patients between two groups； CIBERSORT algorithm was used to perform the immuno-correlation analysis between two groups；multivariate Cox regression analysis and LASSO regression analysis were used to construct the prognostic model； receiver operating characteristic curve （ROC） and K-M survival curve were used to assess the relationship between LRGs and survival and prognosis of the HNSCC patients. The prognostic model was validated by GSE27020， GSE41613，and GSE65858 datasets.The experiment were grouped based on risk score，and immune-related analysis and tumor score analysis were performed. Results The TCGA Database differential analysis results showed that 1 196 LRGs were identified from HNSCC samples； univariate Cox regression analysis selected 27 differentially expressed genes （DEGs） associated with the prognosis of the HNSCC patients. Two different LRGs subtypes （Group 1 and Group 2） were identified according to the prognosis-related genes. The K-M survival curves results showed that the overall survival （OS） of the patients in Group 2 was significantly higher than that in Group 1， and the immune cell expression amount of the patients in Group 2 was also higher than that in group 1. The multivariate Cox regression and LASSO regression analysis results screened out 9 LRGs， including hypoxanthine phosphoribosyltransferase 1 （HPRT1）， amyloid precursor protein （APP）， glycogen phosphorylase L（PYGL），urokinase-type plasminogen activator（PLAU）， cannabinoid receptor 2 （CNR2）， stanniocalcin 2 （STC2）， nucleotide binding oligomerization domain-like receptor protein 1 （NLRP1）， integrin-linked kinase （ILK）， and forkhead box B1 （FOXB1）；the prognostic model was constructed.The K-M and ROC curve results indicated that the expression levels of above 9 genes were associated with the survival and prognosis of the HNSCC patients， providing good 1-year， 2-year， and 3-year survival prediction effect， and the area under ROC curve （AUC） values were all greater than 0.650. Furthermore， the predictive ability of the prognosis model was validated in GSE27020， GSE41613， and GSE65858 datasets. The patients classified based on the risk scores had distinguishable immune statuses. Conclusion The differentially expressed LRGs of HNSCC screened by bioinformatics methods are related to the survival and prognosis of the HNSCC patients； the prognostic model constructed by 9 LRGs can predict the survival status and treatment response of the HNSCC patients.

Objective To analyze the potential therapeutic targets of Huangqin Tang in treatment of colorectal cancer （CRC） by network pharmacology and molecular docking techniques，and to clarify the related molecular mechanism. Methods The active component and target dataset for Huangqin Tang were constructed based on the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform （TCMSP）；the CRC-disease related target dataset was built by Databases such as GeneCards， Online Mendelian Inheritance in Man （OMIM），and pharmacogenetics and Pharmacogenomics Knowledge Base （PharmGKB）. Drug-disease target intersect， Huangqin Tang herbal formula network， and protein-protein interaction （PPI） networks were built by R software， Cytoscape software， and STRING Database； Gene Ontology （GO） functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes （KEGG） signaling pathway enrichment analysis were conducted by R software and Metascape platform；molecular docking validation was performed with AutoDock and PyMOL software to assess the ligand-receptor binding. Results A total of 136 effective active components of Huangqin Tang were screened， and 242 potential targets were identified for treatment of CRC， including 18 core targets. Five core key targets closely related to CRC， identified through signaling pathway analysis， were protein kinase B1（AKT1）， mitogen-activated protein kinase 3 （MAPK3），proto-oncogene FOS，tumor protein p53 （TP53），and proto-oncogene MYC.The GO functional enrichment analysis results mainly involved various biological processes related to cellular stress responses. The KEGG signaling pathway enrichment analysis results showed that potential targets were highly enriched in the cancer pathway； further analysis on CRC core targets via KEGG signaling pathway revealed involvement primarily in pathways related to endocrine resistance， apoptosis， and epidermal growth factor receptor-tyrosine kinase inhibitor （EGFR-TKI） resistance. The molecular docking results showed that the active components of Huangqin Tang， including quercetin， kaempferol， baicalein， 7-methoxy-2-methyl isoflavone， and naringenin， were stably docked with AKT1， MAPK3， FOS， TP53， and MYC， and quercetin exhibited the best binding with AKT1. Conclusion The active components of Huangqin Tang can treat CRC through multi-target and multi-pathway. The core ligand quercetin and AKT1 may exert the therapeutic effect in CRC by regulating the phosphatidylinositol 3-kinase （PI3K）/AKT and mammalian target of rapamycin （mTOR） signaling pathways to influence the cell proliferation， differentiation， and apoptosis processes.

Objective To observe the clinical efficacy of plan-do-check-Act （PDCA） cycle management model combined with pulsed tooth punch applied in maintenance period of the patients with moderate to severe periodontitis， and to provide the theoretical basis for application of the PDCA cycle management model in the periodontitis patients. Methods A total of 50 patients with moderate to severe periodontitis were selected based on predefined inclusion， exclusion， and elimination criteria. The patients were randomly divided into experiment group （n=25） and control group （n=25）. The patients in experiment group underwent maintenance care with pulsed tooth punch in combination with the BASS brushing technique， while the patients in control group maintained oral hygiene with the BASS brushing technique alone.The patients in both two groups were managed with the PDCA cycle management model. The patients were asked to return for follow-up visits at 2， 4， 8， and 12 weeks of self-care， and the personalized corrections and guidance were provided based on the plaque accumulation. The clinical periodontal parameters， including plaque index （PLI）， probing depth （PD），and bleeding index （BI），at 4 and 12 weeks of self-care， as well as the levels of tumor necrosis factor-α （TNF-α） and interleukin-17 （IL-17） in the gingival crevicular fluid of the patients in two groups were observed and recorded. Results After 4 and 12 weeks of self-care， compared with control group，the PLI， PD， and BI of the patients in experiment group were significantly decreased （P<0.01）； compared with baseline， the PLI， PD， and BI of the patients in both two groups at 4 and 12 weeks of self-care were increased （P<0.05 or P<0.01）； Compared with 4 weeks of self-care， the PLI， PD， and BI of the patients at 12 weeks of self-care were increased （P<0.01）. After 4 and 12 weeks of self-care， compared with control group，the levels of TNF-α and IL-17 in gingival crevicular fluid of the patients in experiment group were significantly decreased （P<0.01）； compared with baseline，the levels of TNF-α and IL-17 in gingival crevicular fluid of the patients in two groups at 4 and 12 weeks of self-care were increased （P<0.01）. Conclusion The use of pulsed tooth punch under the PDCA cycle management model can significantly decrease the PLI， PD， BI， and the levels of inflammatory factors in gingival crevicular fluid of the patients with moderate to severe periodontitis，and inhibit the plaque formation and control the gingival inflammation， benefite the maintenance of efficacy of the patients with moderate to severe periodontitis.

Objective To analyze the efficacy of anterior cervical Hybrid surgery and posterior cervical expansive open-door laminoplasty （EODL） in the treatment of multilevel cervical spondylotic myelopathy， and to discuss the selection of surgical methods for the patients with multilevel cervical spondylotic myelopathy. Methods The retrospective analysis was conducted of 70 patients with multilevel cervical spondylotic myelopathy who underwent surgery at Affilated Beijing Traditional Chinese Medicine Hospital of Capital Medical University from July 2017 to July 2020. Based on the different surgical methods， the patients were divided into anterior group （n=35 ）and posterior group（n=35）. The patients in anterior group underwent Hybrid surgery ［anterior cervical discectomy and fusion （ACDF） combined with artificial cervical disc replacement （ACDR）］，and the patients in posterior group underwent EODL. The hospitalization time， operation time， intraoperative blood loss， and postoperative drainage volume of the patients in two groups were recorded； the efficacy was evaluated by Japanese orthopaedic association （JOA） score， JOA improvement rate， neck disability index （NDI）， visual analogue scale （VAS） for pain， and postoperative satisfaction score； the complications of the patients in two groups after surgery were recorded. Results Compared with posterior group， the intraoperative blood loss， postoperative drainage volume， hospitalization time， and operation time of the patients in anterior group were significantly decreased （P<0.01）， and the preoperative score had no significant difference （P>0.05）. At the final follow-up after surgery， compared with posterior group， the JOA score and JOA improvement rate of the patients in anterior group were significantly increased （P<0.01）， and the NDI score and VAS score were significantly decreased （P<0.01）.Compared with before surgery， the JOA scores of the patients in two groups at the final follow-up after surgery were increased （P<0.01）， and the NDI and VAS scores were significant decreased （P<0.01）. The postoperative satisfaction of the patients in two groups was high based on the postoperative satisfaction score.There was no significant difference in the incidence of postoperative complication of the patients between two groups （P>0.05）. Conclusion Both the anterior cervical Hybrid surgery and EODL achieve the satisfactory results in the treatment of multilevel cervical spondylotic myelopathy. Hybrid surgery has the advantages of less bleeding and shorter surgery time， and the most suitable surgical method should be chosen clinically based on the actual situation of the patients.

Objective To analyze the clinical presentations and diagnostic and treatment process of one patient with autoimmune encephalitis（AE） with double positive anti-N-methyl-D-aspartate receptor （NMDAR） and anti-γ-aminobutyric acid B receptor （GABA_BR） secondary to herpes simplex virus encephalitis（HSVE），and to improve the clinicians’ awareness of this disease. Methods The clinical data of one AE patient with double positive anti-NMDAR and anti-GABA_BR secondary to HSVE were collected， the diagnostic and therapeutic processes were summarized， and the relevant literatures were reviewed. Results The patient， a 36-year-old male， developed a headache followed by limb convulsions， and progressed to disturbed consciousness. After admission， the routine biochemistry of the cerebrospinal fluid （CSF） was abnormal， and the herpes simplex virus-1 （HSV-1） IgG antibody showed positive in the CSF； both CSF and serum tests for NMDAR antibodies were positive； the head magnetic resonance imaging （MRI） results showed abnormal signals in the right occipital white matter， leading to the diagnosis of HSVE secondary to anti-NMDAR encephalitis. Several months later， the patient experienced psychiatric behavior abnormalities， cognitive dysfunction， and sleep disorders， and both the serum NMDAR and GABA_BR antibodies showed positive results， prompting the diagnosis of HSVE secondary anti-NMDAR encephalitis and anti-GABA_BR encephalitis. After treatment with steroid pulse therapy and intravenous immunoglobulin （IVIG）， the patient’s condition was improved and the patient was discharged. At one-year follow-up， the patient’s psychiatric symptoms had completely resolved， leaving mild cognitive impairment. Conclusion If the clinical symptoms of the patients recovering from antiviral treatment for HSVE is worsened， secondary AE should be highly suspected；it is important to complete autoimmunity antibody testing as soon as possible for the early diagnosis and treatment to improve the prognosis of the patient.

Objective To discuss the clinical characteristics， diagnosis processes， and treatment methods of one patient with congenital intrabdominal hernia，and to summarize the potential misconceptions during the diagnostic and treatment processes， and to improve the clinicians’ awareness of this disease. Methods The clinical data and auxiliary examination results of one patient with congenital intrabdominal hernia were collected and analyzed， and the related literatures were reviewed. Results The patient， a 65-year-old male， sought care at the local hospital due to upper abdominal pain before 2 d；there were no significant abnormalities in the examination results at the cocal hospital；blood glucose>25 mmol·L^－1.After receiving hypoglycemic， rehydration， and blood purification treatment， the condition of the patient was worsened， presenting with confusion， hypotension， and respiratory distress；the patient admitted in our hospital for further diagnosis and treatment.After admission，the patient was given despite fluid resuscitation， mechanical ventilation， and supportive treatment， but there was no improvement in the symptoms；interventional radiology was performed angiography of the abdominal artery and right femoral vein， which showed no significant vascular abnormalities in the abdomen. An abdominal paracentesis yielded a mixed bloody fluid， suggesting the concealed intraperitoneal disease； exploratory laparotomy was performed. During operation， the intrabdominal hernia with small intestine necrosis and septic shock were diagnosed， and partial small intestine resection， anastomosis， adhesiolysis， and abdominal irrigation and drainage were carried out. The patient had a good recovery and was discharged on the 14th day after operation. Conclusion Congenital intrabdominal hernia is a very rare cause of intestinal obstruction in the adults，and high suspicion for intrabdominal hernia is one of the differential diagnosis for atypical acute abdomen；early multidisciplinary intervention can be lifesaving for the patients.

Objective To conduct the genetic analysis of a family with one patient suffering from juvenile Parkinson’s disease （JP） and discuss the clinical manifestations， genetic mutation characteristics， and treatment plans prompted by PRKN gene compound heterozygous mutations，and to enhance the clinicians’ awareness of this disease. Methods The clinical data of one patient with JP caused by PRKN gene mutations was analyzed， the clinical manifestations and genetic mutation features of the patient were summarized， and the related literatures were reviewed. Results The patient， a 16-year-old male， was admitted to the hospital due to unstable gait， trembling limbs with rigidity in both lower limbs for three years.The examination results revealed a panic gait， clear consciousness， fluent speech， normal muscle strength in limbs， increased “gear-like” muscle tone in both upper limbs， and “lead-pipe” rigidity in both lower limbs；the sensory functions and tendon reflexes were normal. The head， neck， and thoracic magnetic resonance imaging （MRI） results showed no abnormalities. ¹⁸F-fluorodeoxyglucose （¹⁸F-FDG） positron emission tomography/computed tomography （PET/CT）results showed that the head size and shape were normal， the glucose metabolism in the left cerebellum and middle temporal gyrus was slightly decreased， and the glucose metabolism in bilateral thalami， right frontal lobe， parietotemporal lobe， and left medial frontal lobe was increased. The dopamine transporter （DAT） PET/CT results showed that there was no radioactive distribution in the brain cortex and the DAT distribution in the posterior part of both striata was decreased. The whole-exome sequencing results showed the patient had two PRKN gene mutations，such as codons c.8T>A and c.850G>C compound heterozygous mutations，and each mutation was from one parent；the patient’s father carried the c.8T>A mutation， the patient’s mother carried the c.850G>C mutation， and the patient’s sister had the same genetic mutation site as the patient’s father. Conclusion PRKN gene compound heterozygous mutations may be the basis of the disease in this family. Identification of the mutation c.8T>A expands the mutation spectrum of the PRKN gene， and provides the valuable information for the research on the pathogenic genetic mutations of the JP patients.

Objective To discuss the distinctive sonographic feature and the biological behavior of renal angiomyolipoma （RAML）， and to provide the reference for the clinicians to make the accurate diagnosis of RAML. Methods The clinical data of one patient with invasive classical RAML combined with pseudaneurysm formation were collected. The sonographic appearances were analyzed in conjunction with the pathological characteristics to clarify the biological behavior of RAML， and the relevant literatures were reviewed. Results The patient， a 60-year-old female， visited the local hospital due to discomfort in the lumbar area，and received CT examination，and the CT examination results revealed a left renal mass，so the patient came to our hospital. The specialist clinical examinations and laboratory investigations were unremarkable. The ultrasound results indicated an enlarged left kidney with a cystic and solid mass at the upper pole， which featured pseudaneurysm formation （originating from the interlobar arteries）； the enhanced CT image results suggested a high probability of upper pole renal carcinoma combined with aneurysmal formation within the tumor， alongside invasion into the left adrenal gland. The patient underwent laparoscopic radical left nephrectomy， and the postoperative pathology confirmed the diagnosis of invasive classical RAML. Conclusion The classical RAML can exhibit the invasive biological behavior. The pseudaneurysm formation is a special sonographic manifestation of RAML， which can be challenging to differentiate from the other renal tumors.

Objective To confirm the potential etiological factors of congenital aortic stenosis （AS） by genetic analysis on prenatal diagnostic results of the fetus with AS. Methods Amniocentesis for chromosomal G-band karyotyping combinated with single nucleotide polymorphism array （SNP-array） analysis was conducted on the amniotic fluid collected from a 25-week pregnant woman diagnosed as “fetus AS”； chromosome karyotyping was also performed on the peripheral blood of the fetal parents. Results The fetal karyotype analysis showed a chimeric Y-chromosome isobaric double-adherent granules. The SNP-array analysis results revealed a 11.2 Mb duplication in the Yp11.31q11.21 region and a 14.8 Mb deletion in the Yq11.21q11.23 region. Both the parents presented a normal karyotype， suggesting it was a newfound mutation. After extensive genetic counseling， the pregnant woman and her family chose to terminate the pregnancy locally. Conclusion The chromosomal karyotype of the chimeric Y-chromosome isobaric double-adherent granules may be a contributing factor to the AS phenotype in the male fetus. The combined use of chromosomal karyotyping and SNP-array analysis on the amniotic cells is instrumental in the early diagnosis of the disease.

The basement membrane is a specialized extracellular matrix between the epithelium and the mesenchyme. In stratified epithelium, only the basal cells in contact with the basement membrane exhibit the apical-basal polarity, whereas the epithelial cells do being not in contact with the basement membrane do not exhibit the apical-basal polarity. The basement membrane plays an important role in epithelial cell polarization. It is an important extracellular matrix (ECM) structure in the multicellular organisms, is situated between the epithelium and the mesenchyme, and is produced jointly by the epithelial cells and mesenchymal cells. Its components mainly include Laminin, type Ⅳ collagen (Col-Ⅳ), nidogen(NDG), and heparan sulfate proteoglycans (HSPG), and each component plays the different role in influencing the epithelial cell polarity. The network scaffold formed by Col-Ⅳ and Laminin is the main structure of the basement membrane, and the integrity of the structure affects the epithelial cell polarization. This review summarizes the composition and structure of the basement membrane, focuses on its role in epithelial cell polarization and its mechanism, and compiles the current status of biomimetic basement membrane materials that promotes the epithelial cell polarization, and provides the theoretical foundation for further exploration of the establishment and maintenance of epithelial cell polarity.

Early start denver model (ESDM) is a comprehensive early intervention approach for the children with autism spectrum disorder (ASD) between 12-month-old－36-month-old. The model is built upon the theoretical foundations of applied behavior analysis, denver model (DM), and pivotal response treatment, and it is one of the naturalistic developmental behavioral interventions. Compared with the other early intervention methods, ESDM is not limited by the environment of intervention; it encompasses all the areas of development during teaching practice and has been widely adopted for the early intervention of the children with ASD, and achieves the satisfactory therapeutic effect. The ESDM typically uses an intensive one-on-one intervention approach, but variabilities have emerged in its practical application, such as group ESDM(G-ESDM), parent-implemented ESDM (P-ESDM), and peer-mediated ESDM. In particular,G-ESDM and P-ESDM have provided the learning opportunities for more families, showing a broad application prospect. This study reviews the theoretical foundations, teaching models, and the effects of various intervention modalities of the ESDM in the treatment of ASD; combined with the domestic and international research findings,this study offers a reference for further studies on the mechanism of ESDM intervention for ASD.

The gastrointestinal motility disorder of the patients with Parkinson’s disease (PD) occurs in the early stages of this disease, even before the onset of motor symptoms. The gastrointestinal motility disorder is one type of gastrointestinal dysfunction, not only affect the absorption of medication, exacerbating the progression of PD, but also severely impact the quality of life of the patients. Therefore, it is essential to find new therapeutic targets to alleviate PD-induced gastrointestinal dysmotility in order to improve the progression of the disease and the quality of life of the patients. The gastrointestinal motility function is highly dependent on the health of the gut and central nervous regulating the gastrointestinal movements. A healthy gut is closely related to the integrity of the intestinal barrier, gut microbiota, neuroinflammation, and the normal function of enteric neurons responsible for the contraction and relaxation of the gastrointestinal tract. The gut function of the PD patients is compromised to some extent. This review summarizes the effects of the enteric nervous system, central nervous system, and gut microbiota on the development of gastrointestinal motility disorder of the PD patients;it also outlines the current therapeutic methods available and their limitations, with the aim of providing the new insights into the treatment of gastrointestinal motility disorder of the PD patients.

Polycystic ovary syndrome (PCOS) is a heterogeneous disorder closely associated with reproductive endocrine dysfunction in the women. The etiology and pathogenesis of PCOS remain unclear. PCOS is the result of the combination of endocrine metabolic disorders, genetics, and environmental factors. Hyperandrogenemia (HA) and insulin resistance (IR) are the fundamental pathophysiological changes in the development of PCOS, and their interactions exacerbate the clinical manifestations of the PCOS patients. The family aggregation and twin study results confirm the genetic predisposition of PCOS; the genome-wide association study (GWAS) results confirm some risk loci and candidate genes of PCOS. The unhealthy lifestyle habits and environmental endocrine disruptors also play an important role in the progression of PCOS, and the gut microbita is involved in the pathogenesis of PCOS. This article provides a comprehensively retrospective analysis on the recent studies about PCOS,and reviews both internal factors and external factors related to the etiology and pathogenesis of PCOS.