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目的:研究紫铆花素对心肌缺血再灌注损伤的保护作用及其机制。方法:体外建立H9c2心肌细胞缺血再灌注模型,分为正常组、模型组、紫铆花素低、中和高剂量组(10,20和40μM)。检测细胞存活率,LDH释放水平,试剂盒检测MDA、SOD、IL-1和IL-6水平,蛋白印迹法检测Bax,Bcl-2蛋白的表达以及AMPK和GSK-3β磷酸化水平。结果:与模型组比较,紫铆花素能够提高细胞存活率,减少LDH水平,降低MDA、IL-1和IL-6,增加SOD水平。减少Bax,Caspase-3蛋白的表达,增加Bcl-2蛋白的表达,提高Bcl-2/Bax的比值(P<0.05)。同时,紫铆花素能够剂量依赖性的促进AMPK和GSK-3β磷酸化。进一步研究发现,紫铆花素的保护作用以及对GSK-3β的促磷酸化被AMPK抑制剂Compound C抵消。结论:紫铆花素能减轻心肌缺血再灌注损伤,抑制心肌细胞凋亡,其作用机制可能通过激活AMPK/GSK-3β信号通路,减轻氧化应激水平有关。
Objective: To study the protective effect and mechanism of Varisin on myocardial ischemia-reperfusion injury. Methods: H9c2 cardiomyocytes were cultured in vitro and divided into normal group, model group, low, medium and high dose of rivalanin (10, 20 and 40μM). The cell viability, the level of LDH release, the levels of MDA, SOD, IL-1 and IL-6 in the kit were measured. The expressions of Bax and Bcl-2 and the phosphorylation of AMPK and GSK-3β were detected by Western blotting. Results: Compared with the model group, the purple rivagonin could increase cell viability, decrease LDH, decrease MDA, IL-1 and IL-6 and increase the level of SOD. Reduce Bax and Caspase-3 protein expression, increase Bcl-2 protein expression and increase Bcl-2 / Bax ratio (P <0.05). Meanwhile, the proliferation of AMPK and GSK-3βin a dose-dependent manner was inhibited by the purple rivalanin. Further study found that the protection effect of the purple rivet and GSK-3β phosphorylation by the AMPK inhibitor Compound C offset. CONCLUSION: Varisin can reduce myocardial ischemia-reperfusion injury and inhibit cardiomyocyte apoptosis. Its mechanism may be related to the activation of AMPK / GSK-3β signaling pathway and the reduction of oxidative stress.