中国生物工程杂志

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. We used the human dopaminergic SH-SY5Y cells as a cell model. The cells over-expressed the wild-typeα-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-SY5Y-Ctr). After administrating with rotenone about 1or 2 weeks 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 mitochondrial 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.