紫铆花素通过调节AMPK/GSK-3β信号通路抑制心肌缺血再灌注损伤  

Protective Effects and Possible Mechanism of Butein on Myocardial Ischemia Reperfusion Injury

作　　者：段佳林[1,2] 奚苗苗[2] 牟菲[2] 蔺瑞[2] 赵美娜[2] 卫国[2] 文爱东[2] 张恩户[1] 

机构地区：[1]陕西中医药大学中药药理研究室,陕西咸阳712046 [2]第四军医大学西京医院药剂科,陕西西安710032

出　　处：《现代生物医学进展》2017年第14期2616-2621,共6页Progress in Modern Biomedicine

基　　金：国家自然科学基金面上项目(81470174);西京医院学科助推项目(XJZT15M19)

摘　　要：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 investigate the protective effects and possible mechanism of butein on myocardial isehemia/reperfusion injury. Methods： H9c2 cells were divided into normal control group, model group, low-dose, medium-dose and high-dose butein groups （10, 20 and 40 μM）. After the drug was administered to cells for 24h, the myocardial ischemia-reperfusion injury was established. Cell viability, LDH, MDA, SOD, IL-1 and IL-6 were tested. The protein expressions of AMPK, Bax, Bcl-2, and GSK-3β were assayed by western blotting. Results＂ Comparedwith model group, butein could improve the cell survival rate, reduce the release of LDH, decrease the levels of MDA, IL-1 and IL-6, increase the level of SOD, decrease the expression of Bax, Caspase-3, increase the expression of Bcl-2and the ratio of Bcl-2/Bax （P 〈0.05）. In further study, we found that these protective effects were abolished by Compound C. Conclusion： Butein has the protective effects on myocardial ischemia/reperfusion injury in vitro, which can inhibit the myocardial injury through activating AMPK/GSK-3β pathway.

关 键 词：紫铆花素 心肌缺血再灌注 AMPK GSK-313 

分 类 号：R-33[医药卫生] R541.4