Effect of NF-κB signaling pathway mediated by miR-711 on the apoptosis of H9c2 cardiomyocytes in myocardial ischemia reperfusion.

Abstract

The aim of this study was to explore the change of the expression of miR-711 in myocardial ischemia-reperfusion (I/R) injury and the possible mechanism. The cardiomyocyte model of I/R injury was constructed. Real-time quantitative fluorescence polymerase chain reaction (qRT-PCR) and Western blotting were used to detect the expression of miR-711 as well as the mRNA and protein levels of NF-κB (p65). Flow cytometry, CCK-8 kit, and enzyme-linked immunosorbent assay (ELISA) were used to detect the apoptosis, cell viability, and the content of LDH and MDA, respectively. Compared to control cells, the expression levels of miR-711, the mRNA, and protein levels of NF-κB were higher in H9c2 cardiomyocytes of I/R, the apoptosis rate of H9c2 cardiomyocytes of I/R was higher, the levels of LDH and MDA were higher in the supernatant of cell culture, and the cell viability was lower. In comparison to the cells of I/R, the apoptosis rate of H9c2 cardiomyocytes of I/R plus miR-711 inhibitors was lower, the levels of LDH and MDA were lower in the supernatant of cell culture, and the cell viability was higher. In comparison to control cells, the expression level of Bcl-2 was lower, and the expression levels of Bax and Caspase-3 were higher in the cells of I/R. In comparison to the cells of I/R, the expression level of Bcl-2 was lower, and the expression levels of Bax and Caspase-3 were higher in the cells of I/R plus miR-711 inhibitors. Overexpression of miR-711 could promote the expression of NF-κB (p65) in the cardiomyocytes of I/R and accelerate the transportation of NF-κB (p65) into the nucleus, thus promoting the apoptosis of cardiomyocytes.