TRIM59 attenuates inflammation and apoptosis caused by myocardial ischemia reperfusion injury by activating the PI3K/Akt signaling pathway.

Abstract

Myocardial ischemia reperfusion injury (MIRI) is a common factor in heart-related diseases. The aim of this study was to explore the effect of TRIM59 gene on MIRI and its mechanism. Rats were used to construct MIRI models, and TRIM59 gene was overexpressed in myocardium by Entranster technique to detect the effects of TRIM59 on myocardial oxidative stress, myocardial injury, and ATPase. In addition, rat myocardial H9c2 cells were cultured, and a hypoxia-reoxygenation model of H9c2 cells was constructed to detect the effect of TRIM59 overexpression on the inflammation and apoptosis of H9c2 cells. Finally, the PI3K/Akt signaling pathway inhibitor LY294002 was used to study the effect of TRIM59 on the PI3K/Akt signaling pathway. Overexpression of TRIM59 in vivo effectively reduced the expressions of MDA, CK, and LDH, and increased the expression of SOD and the activity of Na+-K+-ATPase and Ca2+-Mg2+-ATPase. In addition, overexpression of TRIM59 in H9c2 cells significantly reduced the expression of inflammatory cytokines (IL-1β, IL-6, and TNF-α) and oxidative stress (ROS) levels. TRIM59 also significantly increased the activity of PI3K/Akt signaling pathway and promoted the phosphorylation of Akt. TRIM59 reduces the level of inflammation and apoptosis of myocardial cells caused by MIRI by activating the PI3K/Akt signaling pathway, thereby reducing myocardial injury.