依达拉奉对硝普钠诱导PC12细胞氧化应激的保护作用

摘要

Aim To investigate the protective effect of edaravone on PC12 cells against oxidative stress induced by sodium nitroprusside, and to explore the potential mechanism. Methods Oxidative stress was induced by sodium nitroprusside on PC12 cells. Cell viability was assessed by MTT, morphological changes were observed by phase-contrast microscopy, and flow cytometry assay was used to determine apoptosis ratio.Meanwhile, the expression of Bax and Bcl-2 was analyzed by western blots. Results Edaravone ( 75 μmol· L-1 ) significantly promoted the cell viability decreased bv sodium nitroprusside. Cell morphology under microscopy showed that edaravone decreased cell debris. Early apoptotic cell was decreased by edaravone and the ration of Bcl-2/Bax was also promoted.Conclusion Edaravone protects PC12 cells from apoptosis induced by sodium nitroprusside, the potential mechanism may be related with its potent free radical scavenging activity to NO, which induces oxidative stress leading cell apoptosis through Bax/Bcl-2 signal pathway.%目的 研究依达拉奉对硝普钠诱导PC12细胞损伤的保护作用,并探讨其作用机制.方法 以500 μmol·L-1硝普钠诱导PC12细胞氧化应激损伤,MTT法测定细胞存活率,倒置显微镜观察细胞形态,流式细胞仪检测细胞凋亡,蛋白免疫印迹检测Bax和Bcl-2表达变化.结果 依达拉奉在25 μmol·L-1能增加氧化应激损伤细胞活力,在75 μmol·L-1其保护作用达到峰值,能明显改善细胞形态结构,减少早期凋亡细胞数目,升高细胞Bcl-2/Bax比值.结论 依达拉奉对硝普钠诱导的PC12细胞损伤具有保护作用,其机制可能与依达拉奉清除NO,抑制线粒体凋亡通路有关.