This study aimed to discover the effect of miR-124/STAT3 axis on the inflammation and cell apoptosis in myocardial infarction (MI) rats. Sprague-Dawley (SD) male rats were selected for establishing MI models and divided into Sham, MI, MI + anti-miR-124 and MI + Ad-miR-124 groups. Cardiac function was detected via echocardiography. Hematoxylin & eosin (HE) and triphenyltetrazolium chloride (TTC) staining were used to observe the pathological changes and infarction area, while transferase (TdT)-mediated D-UTP-biotin nick end labeling (TUNEL) assay was to observe myocardial apoptosis. Enzyme-linked immunosorbent assay (ELISA) was used to determine the serum levels of inflammatory cytokines. Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and western blotting were performed to determine the mRNA and protein levels, respectively. Dual luciferase reporter gene assay revealed that STAT3 was a target gene of miR-124. The expression levels of miR-124 were increased and the pSTAT3/STAT3 ratio was reduced in the MI rats. The rats in the MI group showed enhanced LVEDD and LVESD, reduced LVEF and LVFS, as well as larger myocardial infarction area compared with the Sham group, Besides, IL-1β, IL-6, TNF-α and MCP-1 levels were elevated and the expressions of Bax/Bcl-2 ratio and cleaved caspase-3 were downregulated in MI group. We further found that silencing miR-124 improved cardiac function, reduced infarction area and the levels of inflammatory cytokines, as well as prevented myocardial apoptosis in MI rats. Silencing miR-124 could inhibit the inflammation and apoptosis of myocardial cells, thereby relieving the MI injury via upregulation of STAT3.
Keywords: Cell apoptosis; Inflammation; Myocardial infarction; STAT3; miR-124.
© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.