【摘要】 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.更多还原

【Abstract】 The inhibition of mitochondrial respiratory chain complex I and oxidative damage have been implicated in the pathogenesis of Parkinson’s disease（PD）.To study the alteration of cellular antioxidant capability with complex I impairment,human neuroblastoma SH-SY5Y cells were treated by specific mitochondrial complex I inhibitor rotenone and followed by H₂O₂ exposure.The susceptibility of complex I inhibition cells to H₂O₂ was found to be increased in a dose-dependent manner in cell morphology observation and cell viability detection.Meanwhile,one of antioxidant proteins,thioredoxin,was downregulated following the oxidative stress,which suggests the potential role of thioredoxin as a neuronal injury index as well as a therapeutic target for neuroprotection.更多还原