MiR‑370 inhibits the oxidative stress and apoptosis of cardiac myocytes induced by hydrogen peroxide by targeting FOXO1

Abstract

Myocardial infarction, one of the main factors that threatens human health, leads to cardiac cell death. Myocardial cells suffer ischemia and hypoxia for a long period of time, which can lead to irreversible cell death or apoptosis and cardiac dysfunction. MicroRNAs (miRs) have been reported to play an important role in a wide range of biological processes in cardiac myocytes, which respond to inflammation and oxidative stress. The aim of the present study was to investigate the effect of miR-370 on oxidative stress and apoptosis of cardiac myocytes in ischemic H9C2 cells induced by hydrogen peroxide (H2O2). H9C2 cells were cultured and treated with different concentrations of H2O2 solution. Then, cells were transfected with miR-370 mimic or negative control (NC) mimic, small interfering (si)-RNA-Forkhead box O1 (FOXO1) and NC siRNA. A Cell Counting Kit-8 and flow cytometry assay were conducted to detect cell viability and cell apoptosis. The expression of oxidative stress associated factors were detected by ELISA. The levels of miR-370 and FOXO1 were examined using western blotting and reverse transcription-quantitative PCR. A luciferase reporter gene assay was performed to verify whether FOXO1 was a target gene of miR-370. The results revealed that miR-370 expression was downregulated and FOXO1 expression was increased in H9C2 cells induced by H2O2. Additionally, FOXO1 was proven to be a target of miR-370. The ELISA and flow cytometry assay revealed that miR-370 overexpression and FOXO1 silencing reversed H2O2-induced oxidative stress and apoptosis. The results indicated that miR-370 could inhibit the oxidative stress and apoptosis of H9C2 cells induced by H2O2 by targeting FOXO1. Therefore, miR-370 may be a new therapeutic target for ischemic heart disease.