Abstract
MicroRNAs (miRNAs or miRs) play important roles in cardiovascular disease. miR-21-5p is known to be involved in the regulation of cardiomyocyte injury under high glucose and high fat (HG-HF) conditions, but its mechanism of action remains unclear. In the present study, a cardiomyocyte cell line, H9c2, was treated with 33 mM glucose and 250 µM sodium palmitate for 24, 48, and 72 h to produce HG-HF injury. After treatment, miR-21-5p expression was detected by reverse transcription-quantitative PCR. A miR-21-5p mimic was then constructed and transfected into the cells and the potential molecular mechanism was investigated using Cell Counting Kit-8, TUNEL, flow cytometry and western blot assays. Expression of miR-21-5p was significantly downregulated by HG-HF treatment of H9c2 cells for 24, 48, and 72 h. In subsequent experiments, cells were treated for an intermediate period (48 h). Compared with the control group, HG-HF treatment significantly inhibited H9c2 proliferation and promoted apoptosis, while these effects were significantly reduced in the miR-21-5p mimic. Compared with the control group, HG-HF treatment significantly increased reactive oxygen species, while miR-21-5p mimic significantly reduced this effect. Compared with the control group, HG-HF treatment significantly increased the expression of the pro-apoptotic proteins Bax and phosphorylated (p)-Akt and decreased the expression of the anti-apoptotic proteins Bcl-2, p-PTEN, and p-FOXO3a, while overexpression of miR-21-5p significantly reduced these effects. The results revealed that miR-21-5p inhibited apoptosis and oxidative stress in H9c2 cells induced by HG-HF, likely through the PTEN/Akt/FOXO3a signaling pathway.