γ-Mangostin alleviates myocardial ischemia-reperfusion injury by up-regulating SIRT3

Abstract

Purpose: To determine the effect of γ-mangostin on myocardial ischemia (MI) -induced injury of myocardial cells, and the possible involvement of SIRT3 in myocardial cell apoptosis in Sprague-Dawley rats after ischemia-reperfusion (I/R). Methods: Ischemic reperfusion (I/R) model of rat was established, followed by TTC staining. The serum levels of CK-MB and LDH were also assessed. In addition, inflammatory response and oxidative stress were evaluated by quantitative PCR and enzyme linked immunosorbent assay (ELISA), while cell apoptosis was assessed using TdT-mediated dUTP nick end labeling (TUNEL) assay and western blot. The mechanism of action of γ-mangostin by which it mediated improvement in cardiac injury was investigated by ELISA and western blot. Results: γ-Mangostin attenuated myocardial injury and reduced myocardial inflammation in I/R rats (p < 0.05). In addition, it alleviated oxidative stress in I/R rat myocardial tissues and suppressed apoptosis. Furthermore, γ-mangostin improved myocardial injury probably by targeting SIRT3 (p < 0.05). Conclusion: γ-Mangostin has potentials for use as a therapeutic agent for the treatment of myocardial I/R injury. However, there is a need for clinical trials on the compound.