Journal of Jilin University(Medicine Edition) ›› 2019, Vol. 45 ›› Issue (06): 1212-1217.doi: 10.13481/j.1671-587x.20190604

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Neuroprotective effect of emodin on ischemic stroke model rats and its effect on ERK1/2 signaling pathway

PAN Feng1, GUO Xiaqing2, SHEN Jiangyi3, SU Zhiqiang4   

  1. 1. Department of Neurology, Nanyang Central Hospital, Affiliated Hospital, Zhengzhou University, Nanyang 473000, China;
    2. Department of Neurology, Huaihe Hospital, Henan University, Kaifeng 475000, China;
    3. Department of Intensive Care Unit, Nanshi Hospital, Nanyang City, Henan Province, Nanyang 473000, China;
    4. Department of Neurology, First Clinical Hospital, Harbin Medical University, Harbin 150001, China
  • Received:2019-02-01 Online:2019-12-05 Published:2019-12-05

Abstract: Objective: To study the neuroprotective effect of emodin in the model rats with ischemic stroke and its effect the on extracellular regulated protein kinase1/2 (ERK1/2) signaling pathway, and to explore the mechanism of protective effect of emodin on the ischemic stroke. Methods: A total of 200 rats were randomly divided into sham operation group (n=60 rats), model group (n=70) and emodin group (n=70). The rat models of ischemic stroke were established in model group and emodin group. The rats in emodin group were injected intraperitoneally with emodin 30 min before modeling. The neurological dysfunction scores, cerebral infarction volumes and water contents in brain tissue of the rats in various groups were measured; immunohistochemical staining was used to determine the apoptotic rates of ischemic lateral cortex cells of the rats in various groups;Western blotting method was used to determine the expression levels of Cleaved caspase-3, Bcl-2 related X protein (Bax), B lymphocyte tumor-2 (Bcl-2), ERK1/2 and phosphorylation-ERK1/2 (p-ERK1/2) proteins of the rats in various groups. Results: The rats in sham operation group had no neurological dysfunction and cerebral infarction. The neurological dysfunction score and cerebral infarction volume of the rats in emodin group were significantly lower than those in model group (t=8.331, t=3.538, P<0.05).Compared with model group, the water content in brain tissue of the rats in emodin group was decreased (t=9.507, P<0.05), the apoptotic rate of cerebral cortex cells was decreased (t=57.593,P<0.05), the expression levels of Cleaved caspase-3, Bax, and p-ERK1/2 proteins in ischemic brain tissue were decreased (t=4.088, t=4.463, t=10.659, P<0.05), and the expression level of Bcl-2 protein in ischemic brain tissue was increased (t=5.035, P<0.05). Conclusion: Emodin may inhibit the neuronal apoptosis by inhibiting the ERK1/2 signaling pathway to exert the neuroprotective effect on the rats with ischemic stroke.

Key words: emodin, ischemic stroke, neuroprotection, extracellular regulated protein kinase, apoptosis

CLC Number: 

  • R743.3