Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

α-Mangostin protects against myocardial ischemia reperfusion injury by suppressing the activation of HIF-1α

Hong Jiang¹, Wenli Guo², Dongdong Zhu¹, Wei Zhang¹, Jing Yu¹, Manli Feng¹, Xiaoyu Wang², Xiaopeng Wang², Yanan Jiao³, Chengcheng Wang⁴, Yan Chen¹

¹Department of Cadre Health; ²Department of Emergency; ³Department of Acupuncture and Rehabilitation, Qingdao Hiser Hospital; ⁴Department of Gynecology, Qilu Hospital of Shandong University (Qingdao Campus), Qingdao, Shandong 266000, China.

For correspondence:- Yan Chen Email: cgaws@yahoo.com Tel:+8653283777278

Accepted: 20 December 2019 Published: 31 January 2020

Citation: Jiang H, Guo W, Zhu D, Zhang W, Yu J, Feng M, et al. α-Mangostin protects against myocardial ischemia reperfusion injury by suppressing the activation of HIF-1α. Trop J Pharm Res 2020; 19(1):25-31 doi: 10.4314/tjpr.v19i1.4

© 2020 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the cytoprotective effect of α-mangostin on myocardial tissues in ischemic rats, and the underlying mechanism.

Methods: Histopathological changes in myocardial tissues were determined using inverted microscope. Protein expressions were measured by western blotting, while enzyme-linked immunosorbent assay (ELISA) was used to assay the expression levels of caspase-3, caspase-9 and caspase-8.

Results: Treatment with α-mangostin (20 mg/kg) suppressed production of reactive oxygen species (ROS) and lipid peroxides in myocardial tissues of MI/R rats, and significantly alleviated MI/R injury-mediated reduction in ATP levels in cardiac tissues (p < 0.05). α-Mangostin treatment of MI/R injury rats suppressed HIF-1α activation, and markedly elevated BNIP3 levels, relative to model group. Moreover, MI/R-induced cardiomyocyte apoptosis was significantly alleviated by α-mangostin treatment (p < 0.05). Treatment with α-mangostin also suppressed I/R-induced increases in caspase-8 and caspase-3 activation in myocardial tissues, improved Nrf-2 activation, and promoted HO-1 and GST levels in MI/R injury rats (p < 0.05).

Conclusion: These results suggest that α-mangostin protects rat cardiac tissues from MI/R-induced oxidative damage via reduction of HIF-1α expression, inhibition of ROS generation and suppression of apoptosis. Therefore, α-mangostin may be of therapeutic importance for the management of myocardial ischemia in humans.

Keywords: α-Mangostin, Hypoxia, Inflammation, Nrf-2, Oxidative stress, Reperfusion