中文摘要：

建立稳定表达α-synuclein基因的人神经母细胞瘤细胞株SH-SY5Y细胞，鱼藤酮作用1、2、4周后分别提取各组细胞线粒体，检测其complex Ⅰ功能、线粒体膜肿胀度和超氧阴离子的含量。结果显示在1、2周时过表达α-synuclein基因的细胞与对照组细胞相比，前者的complex Ⅰ的活性高，线粒体膜肿胀度轻，线粒体超氧阴离子的含量少，但4周后，前者的complex Ⅰ活性明显低于后者，线粒体膜肿胀度及线粒体内超氧阴离子的含量均显示前者高于后者。由此可见过表达α-synuclein基因的细胞在早期对鱼藤酮的损伤有一定的抵抗作用，但长期作用后可能有加重损伤的作用。提示PD患者多巴胺能神经元内α-synuclein的增高可能对小剂量鱼藤酮导致的线粒体损伤存在双重调节作用。

英文摘要：

Mitochondrial dysfunction has been implicated in the aetiology of sporadic Parkinson＇s disease but its role in the disease mechanism remains unclear. To investigate the effect of synuclein on mitochondrial dysfunction induced by rotenone. The human dopaminergic SH-SY5Y cells were used as a cell model. The cells over-expressed the wild-type α-synuclein were treated with complex I inhibitor rotenone. The cell viability, complex Ⅰ activity, Mitochondrial swelling and O2^- content were tested at different time point-1w,2w,4w after rotenone treated. CCK-8 test results showed that the cell viability of overexpressed α-synuclein（SH-SY5Y-Syn） was much lower than the control group （SH-SY5 Y-Ctr）. After administrating with rotenone about 1 w or 2w the cell viability of SH-SY5Y-Syn became higher than that of SH-SY5Y-Ctr. On the 4th week the results were contrary to the first 2 weeks. Similar results were got when test the mitochondrial function. In the first 2 weeks after rotenone administrating ,the mitoehondrial function of SH-SY5Y-Syn was better than that of SH-SY5Y-Ctr. This suggest that the α-synuclein could protect the mitochondrial against the injury induced by rotenone in the early stage-1w,2w, while this effect disappeared in the final stage-4w.