利福平通过抑制内质网应激减轻鱼藤酮诱导的PC12细胞损伤

The Protective Effect of Rifampicin on Rotenone-induced PC12 Cells Injury by Inhibiting Endoplasmic Reticulum Stress

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 whether rifampicin protects PC12 cells against rotenone-induced cell injury, and to explore related mechanism based on endoplasmic reticulum stress. Methods ： The Parkinson ＇s disease（PD） cell model was established by rotenone, and rifampicin was added to cells for 2h before rotenone. The viability of PC12 cells was measured by MTT assay. The morphological changes of cells stained by DAPI were observed under fluorescence microscope. The protein levels of GRP78 and cleaved-Caspase12 were determined by Western blot.Results： In cells treated with rifampicin＋ roteone, the viability of PC12 cells was significantly increased（P〈0.01,P〈0.05）, and the morphology of cells was obviously improved. The expression of GRP78 was up-regulated and the expression of cleaved-Caspase12 was decreased（P〈0.05） as compared to those in rotenone group. Conclusion ：Pretreatment with rifampicin protects PC12 cell from rotenone-induced cytotoxicity. One of the protective mechanisms by rifampicin may be correlated with GRP78 up-regulation and cleaved-Caspase12 down-regulation, which inhibits the excessive endoplasmic reticulum stress.