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氧化应激与许多神经退变病有关,而线粒体损伤是氧化应激加剧的重要原因。本文通过细胞活性检测(MTT法)、形态学观察,分析NaN_3对原代培养神经元的损伤作用,并通过RT-PCR半定量检测NaN_3损伤后神经元内疏氧还蛋白(Thioredoxin,Trx)mRNA水平的改变,以阐明这一重要的氧还调节蛋白在神经元损伤过程中的作用。实验表明NaN_3以浓度和时间依赖方式损伤神经元,降低Trx表达水平。提示:神经元内呼吸链受损引起Trx表达减少,从而减弱神经元内氧还调节功能,最终引起神经元损伤、死亡。
Oxidative stress is associated with many neurodegenerative diseases, and mitochondrial damage is an important cause of oxidative stress. In this paper, the damage of NaN 3 on primary cultured neurons was analyzed by MTT assay and morphological observation. Thioredoxin (Trx) mRNA was detected by semi-quantitative RT-PCR after NaN 3 injury Level changes to elucidate the role of this important oxygen regulatory protein in neuronal injury. Experiments show that NaN 3 damages neurons in a concentration- and time-dependent manner and decreases the level of Trx expression. It is suggested that the damage of intrastromal respiratory chain leads to the decrease of Trx expression, which in turn will weaken the function of oxygen regulation in neurons and eventually cause neuronal damage and death.