Cardioprotective effect of miR-214 in myocardial ischemic postconditioning by down-regulation of hypoxia inducible factor 1, alpha subunit inhibitor.

To determine the significance of miR—214 expression in ischemic post—conditioning. Sixty rats were grouped to establish animal models. Immuno— luminescence and chemical methods were used to detect oxidative stress indicators. Hemodynamics indexes were measured by carotid artery intubation, and ischemia and infarction areas by Evans blue and 2,3—5 triphenyltetrazolium chloride(TTC) staining. TargetScan was used for identification and luciferase assays for verification of target genes.miR—214 and hypoxia inducible factor 1, alpha subunit inhibitor (HIF1AN) were analyzed by real—time quantitative polymerase chain reaction. Ischemia reperfusion significantly decreased left ventricular systolic pressure, +dp/dtmax, and —dp/dtmax and increased left ventricular end—diastolic pressure; ischemic post—conditioning had contrasting effects. Compared to the sham group, the ischemic/reperfusion (IR) group showed increased creatine kinase isoenzyme (CK—MB) and malondialdehyde (MDA) in the myocardium and decreased SOD. miR—214 in the IR group was down—regulated, and HIF1AN, up—regulated. Compared with the IR group, the ischemia postconditioning (IPC) group showed decreased CK—MB and MDA in the myocardium and increased SOD. The proportion of infarction area to ischemia area in IPC group declined compared to IR group. miR—214 and HIF1AN in the IPC group showed significant up— and down—regulation, respectively. Ischemic postconditioning can improve myocardial function, reduce myocardial infarction area, and prevent the ischemia reperfusion injury. miR—214 may participate in the protective function of ischemic post—conditioning by down—regulating HIF1AN.