葛根素对心肌细胞氧化应激损伤的保护作用  

Protective effects of Ge Gensu on oxidative stress injury of myocardial cell

作　　者：李宁[1] 郝志梅[2] 崔书霞[3] 熊瑞媛[1] 李继安[4] 马宇杰[5] 田炜[1] 徐菁蔓[1,6] 

机构地区：[1]河北联合大学医学实验研究中心心脏研究所,河北唐山063000 [2]河北联合大学管理学院,河北唐山063000 [3]解放军285医院,河北邯郸056000 [4]河北联合大学中医学院,河北唐山063000 [5]河北联合大学附属开滦医院ICU,河北唐山063000 [6]天津医科大学生理学与病理生理学系,天津300070

出　　处：《中国中医基础医学杂志》2014年第11期1501-1503,1568,共4页JOURNAL OF BASIC CHINESE MEDICINE

基　　金：河北省自然科学基金资助项目(H2012401036);唐山市科技计划项目(131302103z)

摘　　要：目的:探讨葛根素(puerarin,Pue)在心肌细胞氧化应激损伤中的保护作用。方法:利用H2O2处理心肌H9c2细胞,建立氧化应激损伤模型。采用激光扫描共聚焦显微镜成像法测定线粒体膜电位,用MTT法观察Pue对细胞增殖的影响,利用Western blotting法检测Pue对GSK-3β、Akt活性的影响。结果:Pue明显减轻H2O2诱发的心肌细胞线粒体损伤,但PI3K抑制剂渥曼青霉素(wortmannin,Wort)对此作用没有影响;Pue能够增加GSK-3β(Ser9)蛋白的表达,而未增加Akt(Ser473)蛋白的表达。结论:Pue通过使GSK-3β失活,抑制m PTP的开放,从而减轻氧化应激诱发的心肌细胞损伤,而PI3K/Akt信号传导通路并未参与此过程。Objective： To investigate the effects of puerarin in oxidative stress induced myocardial cell injury. Methods： H202was used to induce H9c2 cells＇ oxidative stress injury. Mitochondrial membrane potential （△ψm） was measured by laser scanning confocal microscopy （LSCM）. Cell activity was detected by 3-（4,5 ）-dimethylthiahiazo （-z- yl ）-3,5-di-phenytetrazoliumromide（MTT）. Cellular signaling factors such as GSK-313 and Akt phosphorylation were tested by western blotting. Results： Puerarin markedly decreased the myocardial mitochondrial injury induced by H202 which could not be reversed by PI3K inhibitor wortmannin. Compared to the H202 group, puerarin （0. 1 μM） significantly increased the GSK-3β but not the Akt phosphorylation. Conclusion： Puerarin may prevent oxidative stress-induced H9c2 cells＇ injury by inhibiting mPTP opening via GSK-313. However, PI3K/Akt may not be involved in puerarin induced cardioprotection.

关 键 词：葛根素 氧化应激损伤 线粒体 GSK-3Β AKT 

分 类 号：R331.36[医药卫生—人体生理学]