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丹酚酸B对MPP+所致线粒体损伤PC12细胞的保护作用
杨军岭1,杨侠2*
0
(1. 解放军323医院药剂科, 西安 710054;
2. 陕西省人民医院医务处, 西安 710068
*通信作者)
摘要:
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。
关键词:  帕金森病  丹酚酸B  1-甲基-4-苯基吡啶  PC12细胞  线粒体
DOI:10.3724/SP.J.1008.2015.00685
投稿时间:2015-03-17修订日期:2015-05-08
基金项目:
Protective effects of salvianolic acid B on MPP+-induced mitochondrial injury in PC12 cells
YANG Jun-ling1,YANG Xia2*
(1. Department of Pharmacy, No. 323 Hospital of PLA, Xi'an 710054, Shaanxi, China;
2. Department of Medical Affair, Shaanxi Provincial People's Hospital, Xi'an 710068, Shaanxi, China
*Corresponding authors)
Abstract:
Objective To investigate the protective effects of SalB on 1-methyl-4-phenylpyridinium (MPP+)-induced mitochondrial dysfunction in PC12 cells and the potential mechanism. Methods The injured model of PC12 cells was established by exposing to MPP+ and the mitochondrial function was evaluated by mitochondrial membrane potential (MMP) and mitochondrial ATP synthesis. PCR was used to measure the mitochondrial DNA (mtDNA) content and the expression of PGC-1, NRF-1 and TFAM. The expression of mitochondrial dynamic related proteins was detected by Western blotting analysis. Results SalB significantly attenuated the MPP+-induced decrease in MMP and mitochondrial ATP synthesis(P<0.05), and it significantly increased mtDNA content and the expression of PGC-1, NRF-1 and TFAM mRNA after MPP+ exposure (P<0.05). Moreover, Western blotting analysis showed that SalB significantly increased the expression of Opa-1 and Mfn-1 protein, but decreased that of Drp-1 and Fis-1 after MPP+ treatment(P<0.05). Conclusion SalB can protect PC12 cells against MPP+-induced mitochondrial dysfunction, probably through regulating mitochondrial biogenesis and mitochondrial fusion related proteins.
Key words:  Parkinson disease  salvianolic acid B  1-methyl-4-phenycpyridiniun  PC12 cells  mitochondria