甘草次酸对谷氨酸所致PC12细胞损伤的保护作用及其机理  

The involvement of mitochondria-mediated pathway in protective effect of 18β-glycyrrhe-tinic acid against glutamate-induced PC12 cells apoptosis

作　　者：王立英[1,2] 刘雨萌[1] 金元宝[1,3] 赵明智[1] 夏婷[1] 孟凡欣[1] 

机构地区：[1]吉林大学珠海学院,广东珠海519041 [2]吉林大学生命科学学院,吉林长春130012 [3]吉林农业大学生命科学学院,吉林长春130012

出　　处：《华西药学杂志》2013年第4期353-356,共4页West China Journal of Pharmaceutical Sciences

摘　　要：目的考察甘草次酸对谷氨酸诱导的PC12细胞损伤的保护作用及作用机制。方法使用20 mmol.L-1谷氨酸处理大鼠嗜铬细胞瘤细胞株(PC12),构建细胞凋亡模型。采用药物预处理给药方法,MTT法测定细胞存活率,Fluo-4 AM染色测定胞内钙离子浓度,JC-1染色测定线粒体跨膜电位变化,western blot测定Bcl-2和Bcl-Xl蛋白表达。结果甘草次酸可明显提高谷氨酸诱导的PC12细胞的还原能力,抑制细胞LDH的释放,提高细胞存活率;抑制兴奋性谷氨酸所引起的细胞内钙离子内流;还原谷氨酸引起的线粒体跨膜电位的减弱,增加Bcl-2和Bcl-Xl蛋白的表达量。结论甘草次酸可通过线粒体依赖途径有效抑制谷氨酸诱导的PC12细胞凋亡。OBJECTIVE The experiment is designed to determine the neuro-protective effects and related mechanisms of 18β-glycyrrhetinic acid against glutamate-induced PC12 cells damage.METHODS PC12 cells were treated with 20 mmol·L-1 glutamate to establish apoptotic cell models.MTT method,Fluo-4 AM staining,JC-1 staining and western blot were used to determine the changes of cell viability,intracellular Ca2＋ concentration,mitochondrial membrane potential and the expression of Bcl-2 and Bcl-Xl in PC12 cells,respectively.RESULTS 18β-glycyrrhetinic acid showed significantly reducing capacity against glutamate-induced PC12.Results showed that 18β-glycyrrhetinic acid enhanced the cell viability,inhibited the over-release of LDH,reduced the intracellular Ca2＋ concentration,restored the mitochondrial membrane potential and increased the expression of Bcl-2 and Bcl-Xl.CONCLUSION 18β-glycyrrhetinic acid showed neuro-protective effects against glutamate-induced PC12 cells damage via mitochondrial-dependent pathway.

关 键 词：甘草次酸 谷氨酸 PC12细胞 凋亡 线粒体功能 

分 类 号：R96[医药卫生—药理学]