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

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.