| 张伟 李涛 陈磊 吴雷涛 赵俊杰 高建苑 △ 陈建宗.红景天苷通过PINK1-Parkin 通路在MPP+诱导的SH-SY5Y细胞中维持线粒体形态和功能[J].,2016,16(9):1649-1653 |
| 红景天苷通过PINK1-Parkin 通路在MPP+诱导的SH-SY5Y细胞中维持线粒体形态和功能 |
| Salidroside Maintains Mitochondrial Morphology and Function in MPP+induced SH-SY5Y Cells through PINK1-Parkin Pathway |
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| DOI： |
| 中文关键词: 红景天苷 PINK1 Parkin 线粒体形态 线粒体膜电位 |
| 英文关键词: Salidroside PINK1 Parkin Mitochondrial morphology Mitochondrial membrane potential |
| 基金项目:国家自然科学基金项目（81173590） |
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| 中文摘要: |
| 目的：研究红景天苷（Salidroside, Sal）对在MPP+诱导SH-SY5Y 细胞线粒体形态和功能的影响及其机制。方法：采用3-（4,5-
二甲基噻唑-2）-2，5- 二苯基四氮唑溴盐（3-（4,5-dimethyl-2-thiazolyl）-2,5-diphenyl-2-H-tetrazolium bromide, MTT）检测细胞活性，
MitoTracker Red CMXRos 进行线粒体染色，四甲基罗丹明乙酯（Tetramethylrhodamine ethyl ester, TMRE）检测线粒体膜电位，
Western blot检测PINK1 和Parkin 蛋白表达水平。结果：单纯Sal处理24 h对细胞活性、线粒体形态和MMP 无影响（P>0.05）。
MPP+ （500 uM）处理SH-SY5Y细胞24 h后，与正常组比较，细胞活性、MMP 水平均降低，线粒体长度减短（P<0.01），并发生碎片
化。Sal（25 uM）预处理24 h可以显著抑制MPP+诱导的细胞活性降低（P<0.01），并维持线粒体长度和增加MMP 水平（P<0.01）。
而且，Sal（25 uM）预处理24 h可以显著恢复MPP+诱导的PINK1 和Parkin 蛋白表达水平下降（P<0.01）。结论：体外实验证实Sal
可以保护MPP+诱导的SH-SY5Y 细胞活性降低、线粒体形态和功能异常，而PINK1-Parkin 通路可能是其机制之一，为进一步临
床开发Sal 治疗PD的新药提供实验依据。 |
| 英文摘要: |
| Objective:This study aims to investigate the mechanismof Salidroside (Sal) protecting mitochondrial morphology and
function in MPP+ induced SH-SY5Y cells.Methods:3- (4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay
was used to test the cell activity; MitoTracker Red CMXRos was used to test the mitochondrial morphology; Tetramethylrhodamine ethyl
ester (TMRE) was used to test the mitochondrial membrane potential (MMP) and Western blot method was used to detect the protein level
of PINK1 and Parkin.Results:Sal treatment of 24 h had no effect on cell activity, mitochondrial morphology and MMP (P>0.05). When
compared with the control group, the cell activity and MMP levels were statistically decreased respectively (P<0.01), and the length of
mitochondrial was statistically shortened (P<0.01) and in fragmentation after MPP+ (500 uM) treated 24 h in SH-SY5Y cells. However,
pretreatment with Sal (25 uM) 24 h could significantly inhibit MPP+ induced the decrease of cellular activity (P<0.01), and maintain mitochondrial
length and increase the level of MMP (P<0.01). Moreover, pretreatment with Sal (25 uM) 24 h could significantly inhibit the
MPP+ (500 uM) induced the decrease of protein level of PINK1 and Parkin (P<0.01).Conclusion:Our vitro experiments showed that Sal
could protect the MPP+ induced the decrease of SH-SY5Y cell activity and shortened the length of mitochondrial and in fragmentation.
PINK1-Parkin pathway might be one of the mechanisms. It was provided experimental basis for Sal as a new drug for the treatment of
PD. |
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