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目的探讨丹酚酸B(salvianolic acid B,SalB)对1-甲基-4-苯基吡啶离子(1-methyl-4-phenylpyridinium,MPP+)所致线粒体损伤PC12细胞的保护作用及可能机制。方法采用MPP+处理PC12细胞建立线粒体损伤模型,测定线粒体膜电位和线粒体ATP合成,PCR检测线粒体DNA及PGC-1、NRF-1、TFAM基因表达,蛋白质印迹检测线粒体融合相关蛋白表达变化。结果 SalB能减轻MPP+所致线粒体膜电位下降和线粒体ATP合成减少(P<0.05);SalB能增加MPP+处理后线粒体DNA及PGC-1、NRF-1、TFAM基因表达(P<0.05);SalB增加MPP+处理后Opa-1和Mfn-1蛋白的表达,而抑制Drp-1和Fis-1蛋白的表达(P<0.05)。结论 SalB可能通过调控线粒体生物发生和线粒体融合相关蛋白对MPP+所致线粒体损伤PC12细胞发挥保护作用。
Objective To investigate the protective effect of salvianolic acid B (SalB) on PC12 cells induced by 1-methyl-4-phenylpyridinium (MPP +) and its possible mechanism. Methods Mitochondrial injury model was established by MPP + treatment of PC12 cells. Mitochondrial membrane potential and mitochondrial ATP synthesis were measured. The mitochondrial DNA and PGC-1, NRF-1 and TFAM gene expression were detected by PCR. The expression of mitochondrial fusion related protein was detected by Western blotting. Results SalB could reduce the mitochondrial membrane potential and mitochondrial ATP synthesis induced by MPP + (P <0.05). SalB increased the mRNA expression of mitochondrial DNA and PGC-1, NRF-1 and TFAM (P <0.05) The expression of Opa-1 and Mfn-1 proteins after MPP + treatment inhibited the expression of Drp-1 and Fis-1 proteins (P <0.05). Conclusion SalB may play a protective role in mitochondrial injury induced by MPP + in PC12 cells through the regulation of mitochondrial biogenesis and mitochondrial fusion related proteins.