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中文摘要：
目的研究依达拉奉对硝普钠诱导PCI2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PCI2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Bel—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Bel—2／Bax比值。结论依达拉奉对硝普钠诱导的PCI2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。
英文摘要：
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.
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