麦角甾苷通过PI3K/Akt/GSK3β通路抑制H_2O_2诱导的小鼠胚胎肝细胞凋亡  

Acteoside Protected Hepatocytes from H_2O_2-Induced Apoptosis by PI3K/Akt/GSK3β Pathway

作　　者：赵培[1] 叶杰[2] 闫晓风[2] 王晓玲[2] Zhao Pei Ye Tingjie Yan Xiaofeng Wang Xiaoling(The Public Experiment Pla（form, School of Basic Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China Department of Biology, School of Basic Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China)

机构地区：[1]上海中医药大学基础医学院公共实验平台,上海201203 [2]上海中医药大学基础医学院生物教研室,上海201203

出　　处：《中国细胞生物学学报》2017年第1期13-20,共8页Chinese Journal of Cell Biology

基　　金：国家自然科学基金(批准号:81503367);上海市教委预算内项目(批准号:2012JW01)资助的课题~~

摘　　要：该文建立了H_2O_2诱导小鼠胚胎肝细胞损伤模型,并探讨了麦角甾苷通过PI3K/Akt/GSK3β通路抑制H_2O_2诱导的胚胎肝细胞凋亡作用机制。CCK-8检测细胞存活率,流式细胞术检测细胞凋亡,Western blot法检测Bcl-x L、Bax、Cyt-c、Akt、p-Akt、GSK3β和p-GSK3β蛋白质水平。结果显示,麦角甾苷可通过降低Bax/Bcl-x L比值、抑制线粒体Cyt-c释放、增加Akt和GSK3β蛋白质磷酸化水平来提高细胞存活率、减少凋亡细胞数量。该研究结果表明,麦角甾苷可通过PI3K/Akt/GSK3β通路调节H_2O_2诱导的小鼠胚胎肝细胞凋亡。In the present study, we investigated that acteoside inhibited the H_2O_2-induced apoptosis through PI3K/Akt/GSK3β signal pathway. H2O2 was used to induce injury of fetal hepatocyte from mice. Cell viability was determined by CCK-8 assay, and apoptosis was assayed by flow cytometry. Western blot was used to investigate protein levels of Bcl-x L, Bax, Cyt-c, Akt, p-Akt, GSK3β and p-GSK3β. Compared with H2O2, acteoside can increase the cell viability and decrease the numbers of apoptotic cells. Meanwhile, the ratio of Bax/Bcl-x L downregulated. The release of Cyt-c from mitochondria into cytoplasm inhibited. The phosphorylation of Akt and GSK3β enhanced. These results suggested that acteoside protected fetal hepatocytes of mice from H2O2-induced apoptosis by PI3K/Akt/GSK3β signal pathway.

关 键 词：麦角甾苷 过氧化氢 细胞凋亡 

分 类 号：R285[医药卫生—中药学]