Visfatin relieves myocardial ischemia-reperfusion injury through activation of PI3K/Akt/HSP70 signaling axis

Myocardial ischemia-reperfusion injury (MIRI) is the most common complication of ischemic cardiomyopathy, which severely affects the prognosis of patients. The purpose of this study was to investigate the protective effects of visfatin on the myocardium after ischemia-reperfusion (I/R) and its mechanism.

Sprague Dawley rats were used to construct the MIRI model and visfatin was administrated intraperitoneally in rats to determine the protective effect of visfatin on myocardium after I/R. In addition, visfatin was used to treat rat myocardial cell line H9c2 cells and detect its effect on H9c2 cells. The effect of visfatin on the PI3K/Akt/HSP70 signaling axis in H9c2 cells was also detected to determine the mechanism of the myocardial protection of visfatin.

The damage of cardiomyocytes in MIRI rats pretreated with visfatin was significantly improved compared with untreated MIRI rats. Visfatin also reduced the level of inflammation and apoptosis of cardiomyocytes in MIRI rats, reduced myocardial injury markers, and improved cardiac function. In vitro, visfatin also reduced inflammatory and apoptotic factors in H9c2 cells. In addition, visfatin also promoted the activity of the PI3K/Akt signaling pathway and increased HSP70 expression in H9c2 cells. The inhibition of the PI3K/Akt signaling pathway was found to attenuate the promotion of HSP70 by visfatin. SiRNA-HSP70 also attenuated the protective effect of visfatin on H9c2 cells.

Visfatin reduces the inflammation and apoptosis levels of myocardial cells through the PI3K/Akt/HSP70 signaling axis, thereby reducing I/R-induced myocardial injury.