CircRNA 010567 improves myocardial infarction rats through inhibiting TGF-β1

OBJECTIVE: To observe the intervention effect of circular ribonucleic acid (circRNA) 010567 on myocardial infarction (MI)-induced myocardial fibrosis (MF) in rats, and to explore whether its mechanism of action is related to the regulation on the transforming growth factor-beta 1 (TGF-beta 1) signaling pathway. MATERIALS AND METHODS: The rat model of acute MI was established using ligation of the left anterior descending coronary artery. Model rats were randomly divided into circRNA 010567 siRNA group and Model group, with sham operation group as Control group. The effects of circRNA 010567 on the cardiac function, MF, myocardial apoptosis, mRNA, and protein expression levels of TGF-beta 1 and Smad3 in heart tissues of MI rats were detected using the small animal ultrasound system, Masson staining, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining, reverse transcription-polymerase chain reaction (RT-PCR), and Western blotting, respectively. RESULTS: Compared with Control group, Model group had significantly decreased cardiac function, significantly lower left ventricular ejection fraction (LVEF), and left ventricular fractional shortening (LVFS), markedly increased left ventricular end-diastolic diameter (LVDd), and left ventricular end-systolic diameter (LVDs), severe MF, as well as a significantly higher apoptosis rate of myocardial cells, and evidently increased mRNA and protein levels of TGF-beta 1 and Smad3 in heart tissues. Compared with Model group, circRNA 010567 siRNA group had evidently improved cardiac function, significantly higher LVEF and LVFS, markedly decreased LVDd and LVDs, alleviated MF, a significantly lower apoptosis rate of myocardial cells, and evidently decreased mRNA and protein levels of TGF-beta 1 and Smad3 in heart tissues. CONCLUSIONS: CircRNA 010567 siRNA can improve the cardiac function, alleviate the MF, and inhibit the myocardial apoptosis, there-by further suppressing MI-induced MF, whose mechanism may be related to the inhibition on the TGF-beta 1 signaling pathway.