MiR-34a promotes myocardial infarction in rats by inhibiting the activity of SIRT1.

OBJECTIVE: To investigate the effect of micro ribonucleic acid (miR)-34a regulating silent information regulator 1 (SIRT1) on myocardial infarction (MI) rats. MATERIALS AND METHODS: A total of 30 male, 8-week-old rats were divided into three groups, including: sham group (M group), MI group and MI + miR-34a treatment group (miR group). Tissue morphology in the MI region was observed via hematoxylin-eosin (HE) staining. Myocardial apoptosis in the three groups was detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Furthermore, the protein levels of SIRT1, B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax) in myocardial cells were detected via Western blotting. RESULTS: Compared with M group, left ventricular end-diastolic diameter (LVEDD) and left ventricular end-systolic diameter (LVESD) increased significantly in MI group and miR group (p<0.05), while left ventricular ejection fraction (LVEF) and fractional shortening (FS) decreased obviously (p<0.05). The results of HE staining showed that the inflammatory infiltration of myocardial cells and intercellular collagen fibers significantly increased, and the neuronal damage was remarkably aggravated in MI group and miR group when compared with M group (p<0.05). Compared with MI group, myocardial necrosis, inflammatory cell infiltration and intercellular collagen fibers all increased significantly in miR group (p<0.05). Moreover, the results of TUNEL assay revealed that myocardial apoptosis rate in MI group [(21.35±3.12)%] was remarkably higher than that of M group [(9.53±1.17)%]. Meanwhile, it was significantly higher in miR group [(42.38±3.44)%)] than that of MI group, displaying statistically significant differences (p<0.05). The number of apoptotic cells increased obviously in MI group when compared with M group, while it decreased significantly in MI group when compared with miR group (p<0.05). Besides, the protein levels of SIRT1 and Bcl-2 in myocardial tissues in miR group were remarkably lower than those of M group and MI group (p<0.05). Furthermore, the protein level of Bax in miR group was higher than that of M group and MI group, and there were statistically significant differences (p<0.05). CONCLUSIONS: Overexpression of miR-34a inhibits the activity of SIRT1, thereby promoting the apoptosis of MI.