二甲双胍保护心肌缺血再灌注损伤的分子的机制
he molecular mechanism of metformin on myocardial ischemia-reperfusion injury
目的:验证二甲双胍对心肌缺血再灌注损伤的保护作用,并探讨其相关的分子机制。方法:利用Langendoff离体灌流实验,测定大鼠左心室功能,心脏梗死面积,心肌酶释放及通过western blot技术检测凋亡相关蛋白的表达水平。结果:二甲双胍明显提高了心肌缺血再灌注过程中的左心室功能,减少了心肌梗死面积和灌流液中CK-MB的释放,同时二甲双胍也显著上调了组织细胞中MnSOD的蛋白表达,减少凋亡蛋白bax的表达 和TUNEL染色细胞阳性率。结论:二甲双胍对心肌缺血再灌注损伤具有保护作用,其作用机制与上调抗氧化酶及下调凋亡蛋白进而减少细胞凋亡有关。
im: The objective was to examine the protective effect of metformin (Met) on myocardial ischemia-reperfusion (IR) injury and It's molecular mechanism. Methods: Rat Langendorff IR test was used in this study, Left ventricular (LV) function, infarct size, CK-MB release and TUNEL staining were performed, Meanwhile, western blot was used to examine the expression of antioxidant enzymes and apoptotic proteins in vitro. Results: Met treatment significantly improved LV function, reduced infarct size and CK-MB release in comparison with IR group. Up-regulated expression of MnSOD, as well as down-regulated expression of apoptotic proteins. Decreased TUNEL staining positive cells were also observed in Met group. Conclusion: Met exerted protective effect on myocardial IR injury, and this effect was related to the up-regulation of antioxidant enzymes and down-regulation of apoptotic proteins.
王小玲、漆智、杨磊
基础医学内科学
二甲双胍心肌缺血再灌注抗氧化蛋白
MetforminMyocardial ischemia reperfusion injuryAntioxidant enzyme
王小玲,漆智,杨磊.二甲双胍保护心肌缺血再灌注损伤的分子的机制[EB/OL].(2016-05-30)[2025-08-16].http://www.paper.edu.cn/releasepaper/content/201605-1535.点此复制
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