Abstract: Objective To investigate the effect of miR-26a on myocardial ischemia-reperfusion (I/R) injury in rats. Methods Rats were randomly divided into control group (n=20),I/R group (n=20) and siRNA group(n=20). Seven days before the establishment of I/R model, miR-26a siRNA was injected into tail vein to silence endogenous miR-26a. Ejection fraction (EF%) and shortening fraction (FS%) were measured by echocardiography.The infarct size was measured by TTC.The morphology of cardiomyocytes was detected by HE staining.TUNEL assay was used to detect the level of cardiomyocyte apoptosis.Western blot was used to detect the expression of Bcl-2 related X protein (Bax), caspase-3 and Rho/RhoA signaling pathway related proteins. Results The expression of miR-26a in I/R group was significantly higher than that in control group (P＜0.05).The EF% and FS% of siRNA group were significantly improved (P＜0.05).In siRNA group, the severity of myocardial infarction caused by I/R was significantly reduced, and the percentage of myocardial infarction area was increased from 43.08%±2.43% to 21.54%±1.82% (P＜0.05).In siRNA group, the myofilaments were arranged orderly, the degree of myocardial necrosis was low, and the cell edema was significantly alleviated compared with I/R group.The level of cardiomyocyte apoptosis in siRNA group was significantly lower than that in I/R group (P＜0.05),and the expression levels of Bax and caspase-3 were also significantly decreased (P＜0.05).Inhibition of miR-26a could significantly reduce the expression of Rho/RhoA signaling pathway protein during I/R (P＜0.05). Conclusions miR-26a silencing may inhibit I/R-induced cardiomyocyte apoptosis by reducing expression of Rho/RhoA signaling pathway protein.

Key words: myocardial ischemia-reperfusion injury, miR-26a, myocardial cells, apoptosis