Abstract
To investigate the effect of micro ribonucleic acid (miR)-101a on myocardial cell apoptosis in the rat model of acute myocardial infarction (AMI) and its regulatory mechanism. A total of 30 Sprague-Dawley (SD) rats were randomly divided into the Sham group, Model group, and miR-101a mimic group, with 10 rats in each group. The rat model of AMI was established by the ligation of the anterior descending coronary artery. The rat left ventricular end-diastolic volume (LVEDV) and left ventricular end-systolic volume (LVESV) were detected using a color Doppler ultrasonic apparatus. Subsequently, the miRNA online database (TargetScan) was adopted to predict miRNAs that could be able to regulate TGF-β1. Hematoxylin and eosin (H&E) staining was conducted to reveal the histopathological morphology changes in the rat heart. The serum levels of cysteinyl aspartate specific proteinase-3 (Caspase-3) and Bcl-2-associated X protein (Bax) in rats were detected via enzyme-linked immunosorbent assay (ELISA). Moreover, the expression levels of the transforming growth factor-beta l (TGF-β1) and c-Jun N-terminal kinase (JNK) in rat heart were measured via Western blotting. Through searching miRNA database, miR-101a and TGF-β1 messenger RNAs (mRNAs) had binding sites in the 3' untranslated region (3'UTR). Compared with those in Sham group, the rat LVEDV and LVESV were notably elevated, the histopathological morphology of the heart was seriously damaged, the apoptotic rate of myocardial cells and the levels of TGF-β1 and JNK proteins significantly increased in the Model group. Additionally, compared with those in the Model group, the LVEDV and LVESV of rats in miR-101a mimic group were significantly reduced, the histopathological morphology of the heart was markedly improved, and the apoptotic rate and the levels of TGF-β1 and JNK in rat heart were remarkably decreased. The myocardial cell apoptosis in AMI rats can be suppressed by overexpression of miR-101a by inhibiting the TGF-β1/JNK signaling pathway.
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