Xiaoping Dong,
Jiangfeng Zhu
General Medicine Ward, The First People's Hospital of Fuyang Hangzhou, Hangzhou, Zhejiang Province 311400, China;
For correspondence:- Jiangfeng Zhu
Email: jiang_fz0531@163.com Tel:+8657161758062
Accepted: 29 October 2022
Published: 30 November 2022
Citation:
Dong X, Zhu J.
γ-Mangostin alleviates myocardial ischemia-reperfusion injury by up-regulating SIRT3. Trop J Pharm Res 2022; 21(11):2309-2315
doi:
10.4314/tjpr.v21i11.6
© 2022 The authors.
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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.
Keywords: Myocardial ischemia (MI), γ-Mangostin, Oxidative stress, Apoptosis, SIRT3, Inflammatory response