【摘要】 目的通过研究PC12细胞抗氧化应激的氧化还原因子-1(apurinic/apyrimidimic endonuclase/redox factor1,APE/Ref-1)分子在过氧化氢和谷氨酸损伤过程中表达水平的变化,探讨谷氨酸对神经细胞损伤的分子机制。方法以PC12细胞作为神经细胞模型,以200和400μmol/L浓度的过氧化氢或以10和20mmol/L谷氨酸钠处理PC12细胞,用噻唑蓝法(MTT法)检测细胞的损伤程度,以Western blot方法测定APE/Ref-1表达水平。结果过氧化氢对PC12细胞的APE/Ref-1蛋白表达具有诱导作用。谷氨酸对PC12细胞的APE/Ref-1蛋白表达无影响。结论谷氨酸对PC12细胞的损伤过程中,所产生的氧化应激作用的水平很低,远不足以引起抗氧化应激的APE/ref-1蛋白的代偿反应。更多还原

【Abstract】 Objective Effect of hydrogen peroxide（H₂O₂） and glutamate on the expression of apurinic/apyrimidimic endonuclase/redox factor 1（APE/ref-1） were observed,while the molecular mechanism of the nervous cells injured by glutamate was investigated.Methods As nervous cell model,PC12 cells were treated with 200 and 400 μmol/L of H₂O₂, or 10 and 20 mmol/L of glutamate,and the injury of PC12 cells was assessed by MTT. The expression of APE/ref-1 in PC12 cells was detected by Western blot.Results 200 and 400 μmol/L of H₂O₂ induced the expression of APE/ref-1 in PC12 cells,but 10 and 20 mmol/L of glutamate had no effect on the expression of APE/ref-1 in PC12 cells.Conclusion The level of oxidative stress in PC12 cells injured by glutamate is so low that the adaptive expression of anti-oxidative APE/ref-1 protein can not be induced.更多还原