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目的:探讨利福平对鱼藤酮诱导PC12细胞损伤的保护作用,并从内质网应激的角度阐明其作用机制。方法:用鱼藤酮诱导PC12细胞构建帕金森病模型,经利福平预处理,MTT法检测细胞存活率,DAPI荧光染色法观察细胞凋亡,Western blot检测GRP78及cleaved-Caspase12的表达变化。结果:与鱼藤酮组相比,利福平加鱼藤酮处理组细胞活力明显提高(P<0.01,P<0.05),细胞的凋亡形态明显改善,GRP78的表达增加(P<0.05),cleaved-Caspase12的表达降低(P<0.05)。结论 :利福平保护PC12细胞免受鱼藤酮诱导的细胞损伤,其保护机制可能与通过上调GRP78及下调cleaved-Caspase12从而抑制过度的内质网应激有关。
Objective: To investigate the protective effect of rifampicin on rotenone-induced injury in PC12 cells and elucidate its mechanism of action from the perspective of endoplasmic reticulum stress. Methods: Parkinson’s disease model was induced by rotenone in PC12 cells. Pretreatment with rifampin, cell survival rate by MTT assay, apoptosis by DAPI staining, and the changes of GRP78 and cleaved-Caspase12 by Western blot. Results: Compared with rotenone group, the viability of cells treated with rifampicin and rotenone increased significantly (P <0.01, P <0.05), and the apoptotic morphology of the cells was significantly improved, the expression of GRP78 increased, cleaved-Caspase12 (P <0.05). CONCLUSION: Rifampicin protects PC12 cells from rotenone-induced cell injury, and its protective mechanism may be related to the inhibition of excessive endoplasmic reticulum stress by up-regulating GRP78 and down-regulating cleaved-Caspase12.