Abstract:

To explore the influence of isoflurane in apoptosis and endoplasmic reticulum stress (ERS) of PC12 cells of the rats  induced by amyloid β-protein 25-35 (Aβ25-35),and to clarify its mechanism.Methods The PC12 cells were randomly divided into normal control group,10  μmol•L-¹ Aβ25-35 group (Aβ group),2% isoflurane group (Iso group),and 2% isoflurane combined with  10  μmol•L^-1 Aβ25-35 group(Iso+Aβ  group).The survival rates  of the PC12 cells in various groups were determined by MTT assay;the apoptotic morphology of the  PC12 cells was detected by Hoechst 33342 staining method;Western blotting method was performed to observe the expression levels of endoplasmic reticulum molecular chaperone glucose regulation protein 78(GRP78) and ERS associated apoptosis signal protein C/EBP homologous protein(CHOP),phosphorylated amino terminal protein kinase(p-JNK),and caspase-12 of PC12 cells.Results Compared with normal control group,the  survival rates of the PC12 cells  in Aβ group and Iso group were decreased significantly(P<0.05),but the  apoptotic rates of the PC12 cells were significantly increased (P<0.05),the expression levels of  GRP78 and ERS associated apoptotic signal protein CHOP,p-JNK and caspase-12 were increased significantly (P<0.05).Compared with Aβ group,the  survival rate of the  PC12 cells  in Iso+Aβ group was decreased significantly(P<0.05),and the apoptotic rate was significantly increased (P<0.05),and the expression levels of  GRP78,  CHOP,p-JNK, and caspase-12 were increased significantly (P<0.05).Conclusion Isoflurane could aggravate the apoptosis of PC12 cells of the  rats induced by Aβ25-35,and the  mechanism may be  involved in activation of ERS and ERS associated apoptosis signal pathway.

Key words: isoflurane, Alzheimer&rsquo, s disease, PC12 cells, endoplasmic reticulum stress, apoptosis