MiR-181a affects myocardial ischemia-reperfusion injury in rats via regulating akt signaling pathway.

Abstract

The aim of this study was to explore the influence of the micro ribonucleic acid (miR)-181a on myocardial ischemia-reperfusion injury (MIRI) in rats by regulating the protein kinase B (Akt) signaling pathway. A total of 30 male Sprague-Dawley rats were randomly divided into three groups, including: sham operation group (Sham group), ischemia-reperfusion group (I/R group), and miR group (MiR-181a group). The model of myocardial ischemia-reperfusion was successfully established in rats. The concentration of blood nitric oxide (NO) was detected by the relative kits. Myocardial apoptosis in rats of the three groups was detected using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Furthermore, the expressions of myocardial cell apoptosis-related proteins and tumor necrosis factor-α (TNF-α), and the degree of Akt phosphorylation were determined by Western blotting. Compared with Sham group and miR-181a group, I/R group exhibited significantly elevated left ventricular end-diastolic pressure (LVEDP) (p<0.05). However, the left ventricular end-systolic pressure (LVESP), stroke work (SW), differential pressure (DP), end-systolic pressure-volume relationship (ESPVR), and end-diastolic pressure-volume relationship (EDPVR) significantly decreased in the I/R group (p<0.05). In comparison with miR-181a group, the apoptosis index of myocardial cells was remarkably elevated in the I/R group, showing statistically significant differences (p<0.05). The protein bands were analyzed using the Quantity One detection software. The results demonstrated that, compared with the Sham group, I/R group showed significantly elevated expressions of cysteine-aspartic protease (Caspase)-3 and TNF-α in rat myocardial tissues (p<0.05). However, the protein levels of Akt and endothelial NO synthase (eNOS) phosphorylation and NO in rat myocardial cells were significantly down-regulated (p<0.05). MiR-181a activates Akt to promote the phosphorylation of its downstream protein eNOS, inhibit the apoptosis of myocardial cells, and alleviate MIRI.