一氧化氮诱导PC12细胞凋亡及人参皂苷Rg1的保护作用

Nitric oxide induced PC12 cells apoptosis and the protective effect of ginenoside Rg1

目的 探讨一氧化氮诱导PC12细胞凋亡及人参皂苷Rg1保护作用的可能机制。 方法 DNA凝胶电泳观察DNA的断裂情况 ,流式细胞仪检测线粒体跨膜电位 ,West ernblotting检测胞浆细胞色素C和活化型半胱氨酸蛋白水解酶caspase 3P2 0 水平。结果 一氧化氮供体SNAP(5 0 0μmol·L-1)可诱导PC12细胞凋亡 ,细胞线粒体跨膜电位明显下降、胞浆细胞色素C水平增加及caspase 3得到激活 ;预先经过 5 0、10和 2 0 μmol·L-1等浓度人参皂苷Rg1处理后 ,SNAP诱导的PC12细胞凋亡明显减少 ,同时明显减弱SNAP对细胞线粒体跨膜电位、胞浆细胞色素C水平及cas pase 3激活的影响。 结论 人参皂苷Rg1可抑制一氧化氮诱导PC12细胞凋亡 ,其作用机制可能与其稳定细胞线粒体跨膜电位、减少线粒体细胞色素C向胞浆释放及抑制cas pase

AIM To explore the possible mechanism of nitric oxide (NO) induced PC12 cells apoptosis and the protective effect of ginsenoside Rg1. METHODS DNA fragmentation was observed by gels electrophoresis and flow cytometric assay was performed to determine the mitochondral membrance potential in PC12 cells. The cytosolic cytochrome c and cleaved caspase 3 P 20 were detected with Western blotting assay. RESULTS 500 μmol·L -1 NO donor S nitroso N acetyl penicillamine (SNAP) induced PC12 cells apoptosis, decreased mitochondral membrance potential, increased cytosolic cytochrome c and activated caspase 3. After pretreatment with ginsenoside Rg1 at the concentration of 5, 10 or 20 μmol·L -1 , the apoptosis induced by SNAP was decreased markedly, and the mitochondral membrance potential decreased, the release of cytochrome c and the activation of caspase 3 were attenuated, too. CONCLUSION Rg1 might protect against NO induced apoptosis in PC12 cells and this effect might be attributed to its stabilizing the mitochondral membrance and its inhibiting of the release of cytochrome c and activation of caspase 3.