MicroRNA-26b-5p表达水平与心肌梗死和细胞凋亡的相关性

Correlation between MicroRNA-26b-5p Expression Level and Myocardial Infarction and Apoptosis

心肌缺血再灌注(I/R)可进一步导致心肌细胞的凋亡和坏死。越来越多的证据表明,microRNA(miRNA)参与了与心肌I/R相关的病理和生理过程。本研究旨在考察microRNA-26b-5p(miR-26b-5p)表达水平与心肌梗死和细胞凋亡的相关性。本研究建立了小鼠心肌I/R模型和缺氧/复氧(H/R)心肌细胞模型(H9C2细胞),检测了miR-26b-5p在I/R小鼠心肌组织和H/R心肌细胞中的表达,并分析了上调miR-26b-5p的表达在体内和体外对心肌细胞凋亡的影响及机制。研究显示,在H/R H9C2细胞和I/R小鼠模型心肌组织中miR-26b-5p的表达水平明显降低。miR-26b-5p的过表达减轻了I/R小鼠模型心肌损伤并在体内和体外抑制了心肌细胞凋亡。此外,丝裂原活化蛋白激酶6(MAPK6)为miR-26b-5p的直接靶标,miR-26b-5p负调节MAPK6的表达。在H/RH9C2细胞中MAPK6的上调抑制了miR-26b-5p对心肌细胞的保护作用。研究结果表明,miR-26b-5p通过靶向MAPK6抑制心肌细胞凋亡从而发挥心脏保护作用。

Myocardial ischemia-reperfusion(I/R)can further cause apoptosis and necrosis of myocardial cells.There is increasing evidence that microRNA(miRNA)is involved in pathological and physiological processes related to myocardial I/R.The purpose of this study was to investigate the correlation between microRNA-26 b-5 p(miR-26 b-5 p)expression level and myocardial infarction and apoptosis.In this study,a mouse myocardial I/R model and hypoxia/reoxygenation(H/R)cardiomyocyte model(H9 C2 cells)were established,the expression of miR-26 b-5 p in I/R mouse myocardium and H/R cardiomyocytes was detected,and the effect and mechanism of up-regulated miR-26 b-5 p expression on cardiomyocyte apoptosis in vivo and in vitro were analyzed.Studies showed that miR-26 b-5 p expression levels were significantly reduced in H/R H9 C2 cells and myocardial tissues in I/R mouse model.The overexpression of miR-26 b-5 p alleviated myocardial injury in the I/R mouse model and inhibited cardiomyocyte apoptosis in vivo and in vitro.In addition,mitogen-activated protein kinase 6(MAPK6)was a direct target of miR-26 b-5 p,and miR-26 b-5 p negatively regulated the expression of MAPK6.In H/R H9 C2 cells,the up-regulation of MAPK6 inhibited the protective effect of miR-26 b-5 p on cardiomyocytes.The results indicate that miR-26 b-5 p inhibits cardiomyocyte apoptosis by targeting MAPK6,thereby exerting cardioprotective effects.