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帕金森病(PD)的发病机制与线粒体呼吸链复合物I(complex I)活性降低以及氧化应激损伤密切相关.使用complex I特异性抑制物鱼藤酮,损伤人神经母细胞瘤SH-SY5Y细胞后,给予H2O2造成氧化应激损伤,以研究细胞抗氧化损伤能力变化的可能机制.结果表明,鱼藤酮处理后,细胞对H2O2所致氧化损伤的易感性增高,且细胞形态及细胞存活率的改变与鱼藤酮浓度呈量效关系.与此同时,细胞内抗氧化蛋白之一,硫氧还蛋白(thioredoxin)水平在细胞损伤时明显下降.以上结果表明,线粒体complex I抑制对细胞氧化应激易感性的影响可能与胞内硫氧还蛋白水平降低有关,提示硫氧还蛋白在诊断神经元损伤和神经保护中有一定的运用前景.
The pathogenesis of Parkinson's disease (PD) is closely related to the decrease of mitochondrial respiratory chain complex I activity and oxidative stress injury.Using complex I specific inhibitor rotenone and injuring human neuroblastoma SH-SY5Y cells , And oxidative stress injury induced by H2O2 to study the possible mechanism of changes in cell antioxidant capacity.The results showed that the susceptibility of cells to oxidative damage induced by H2O2 increased after treatment with rotenone and the change of cell morphology and cell survival rate was associated with Rotenone concentrations in a dose-effect relationship.At the same time, one of the intracellular antioxidant proteins, thioredoxin levels decreased significantly in cell injury.The above results show that mitochondrial complex I inhibit the susceptibility of cells to oxidative stress The effect may be related to the decrease of intracellular thioredoxin level, suggesting that thioredoxin may have certain application prospect in the diagnosis of neuronal damage and neuroprotection.