Mangiferin attenuates myocardial ischemia-reperfusion injury via MAPK/NRf-2/HO-1/NF-κB in vitro and in vivo

29Citations
Citations of this article
17Readers
Mendeley users who have this article in their library.

This article is free to access.

Abstract

The aim of this study was to investigate the cardioprotective effect of mangiferin (MAF) in vitro and in vivo. Oxidative stress and inflammatory injury were detected in coronary artery ligation in rats and also in hypoxia-reoxygenation- (H/R-) induced H9c2 cells. MAF inhibited myocardial oxidative stress and proinflammatory cytokines in rats with coronary artery occlusion. The ST segment of MAF treatment groups also resumed. Triphenyltetrazolium chloride (TTC) staining and pathological analysis showed that MAF could significantly reduce myocardial injury. In vitro data showed that MAF could improve hypoxia/reoxygenation- (H/R-) induced H9c2 cell activity. In addition, MAF could significantly reduce oxidative stress and inflammatory pathway protein expression in H/R-induced H9c2 cells. This study has clarified the protective effects of MAF on myocardial injury and also confirmed that oxidative stress and inflammation were involved in the myocardial ischemia-reperfusion injury (I/R) model.

Cite

CITATION STYLE

APA

Liu, K., Wang, F., Wang, S., Li, W. N., & Ye, Q. (2019). Mangiferin attenuates myocardial ischemia-reperfusion injury via MAPK/NRf-2/HO-1/NF-κB in vitro and in vivo. Oxidative Medicine and Cellular Longevity, 2019. https://doi.org/10.1155/2019/7285434

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free