MiR-125b Improves acute myocardial infarction in rats by regulating P38/Sirtl/P53 signaling pathway

The aim of this study was to investigate the differential expression of micro ribonucleic acid (miR)- 125b in acute myocardial infarction (AMI) cases, and to explore the mechanism by which it affects cardiac function. Sprague-Dawley rats were used for AMI modeling, and the expression of miR-125b in the myocardial tissues of AMI rats was detected via fluorescence quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Thereafter, the target genes of miR-125b were collected and uploaded to WenGestalt for gene ontology (GO) and pathway enrichment analyses. In-vitro experiments were then applied to determine the p38-sirtuin 1 (Sirt1)-p53 expression change and cardiomyocyte apoptosis under down-regulation of miR-125b. Next, the interaction between miR-125b and its target genes was verified by luciferase reporter gene assay. The expression of miR-125b in the cardiac tissues was decreased in theAMI group compared with that in the Sham group (p<0.05). The luciferase reporter gene assay confirmed that p38 was the target gene of miR-125b. Furthermore, the down-regulated expression of miR-125b in H9C2 cells up-regulated the protein expressions of p38 and phosphorylated p38, thus activating the Sirt1-p53 signaling pathway. Moreover, the down-regulation of miR-125b expression in H9C2 cells gave rise to the elevated apoptosis rate, and the down-regulated expression of miR-125b induced cardiomyocyte apoptosis through activating the p38-Sirt1-p53 signaling pathway.