Effect of exosome-carried miR-30a on myocardial apoptosis in myocardial ischemia-reperfusion injury rats through regulating autophagy.

Abstract

To explore the effect of exosome-carried micro-ribonucleic acid-30a (miR-30a) on myocardial apoptosis in rats with myocardial ischemia-reperfusion injury (MIRI) and its possible regulatory mechanism. The MIRI rat model was established via ligation of the left anterior descending coronary artery. A total of 30 Sprague-Dawley (SD) rats were randomly divided into Sham group, Model group, and miR-30a inhibitor group. The pathological changes in heart tissues in MIRI rats were detected via hematoxylin-eosin (HE) staining. The levels of serum aspartate aminotransferase (AST) and creatine phosphokinase (CPK) in MIRI rats were detected using the biochemical method. The content of serum malondialdehyde (MDA) and superoxide dismutase (SOD) was detected via enzyme-linked immunosorbent assay (ELISA). Moreover, the apoptosis of heart tissues in MIRI rats was detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. The protein levels of ULK1 and Beclin-1 were detected via Western blotting. Compared with those in the Sham group, the pathological injury of heart tissues was severe, the levels of serum AST and CPK were increased, the content of MDA was decreased, the content of SOD was increased, the apoptotic rate of heart tissues was significantly increased, and the protein levels of ULK1 and Beclin-1 in heart tissues were also significantly increased in Model group. Compared with those in the Model group, the pathological injury of the heart tissues was alleviated, the levels of serum AST and CPK were declined, the content of MDA was increased, the content of SOD was decreased, the apoptotic rate of heart tissues, and the protein levels of ULK1 and Beclin-1 in heart tissues also significantly declined. The exosome-carried miR-30a inhibitor can suppress the myocardial apoptosis in MIRI rats by reducing autophagy.