依达拉奉对硝普钠诱导PC12细胞氧化应激的保护作用

Neuroprotective effects of edaravone against oxidative stress on sodium nitroprusside-induced PC12 cells

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500μmol.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25μmol.L-1能增加氧化应激损伤细胞活力,在75μmol.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。

Aim To investigate the protective effect of edaravone on PC12 ceils against oxidative stress in- duced by sodium nitroprusside, and to explore the po- tential mechanism. Methods Oxidative stress was in- duced by sodium nitroprusside on PC12 cells. Cell via- bility 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 ana- lyzed by western blots. Results Edaravone （75 trmol ~ L-1） significantly promoted the cell viability de- creased by sodium nitroprusside. Cell morphology un-der microscopy showed that edaravone decreased cell debris. Early apoptotic cell was decreased by edara- vone and the ration of Bcl-2/Bax was also promoted. Conclusion Edaravone protects PC12 cells from ap- optosis 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.