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.

本研究旨在探讨miR-124/STAT3轴对心肌梗死（MI）大鼠炎症和细胞凋亡的影响。选择Sprague-Dawley（SD）雄性大鼠建立MI模型，分为Sham组、MI组、MI+anti-miR-124组和MI+Ad-miR-124组。通过超声心动图检测心脏功能。苏木精-伊红（HE）和氯化三苯基四唑（TTC）染色观察病理变化和梗死面积，转移酶（TdT）介导的D-UTP-生物素缺口末端标记（TUNEL）法观察心肌细胞凋亡。采用酶联免疫吸附测定（ELISA）测定血清炎症细胞因子水平。进行定量逆转录酶聚合酶链反应（qRT-PCR）和蛋白质印迹分别测定mRNA和蛋白质水平。双荧光素酶报告基因检测显示STAT3是miR-124的靶基因。 MI大鼠中miR-124的表达水平升高，pSTAT3/STAT3比值降低。与Sham组相比,MI组大鼠LVEDD、LVESD增强,LVEF、LVFS降低,心肌梗死面积增大,IL-1β、IL-6、TNF-α、MCP-1水平升高MI组Bax/Bcl-2比值和cleaved caspase-3表达下调。我们进一步发现，沉默 miR-124 可改善 MI 大鼠的心功能、减少梗死面积和炎性细胞因子水平，并防止心肌细胞凋亡。沉默miR-124可以抑制心肌细胞的炎症和凋亡，从而通过上调STAT3来减轻心肌梗死损伤。