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Evidence-Based Complementary and Alternative Medicine
Volume 2017 (2017), Article ID 4534387, 10 pages
Research Article

Guanxintai Exerts Protective Effects on Ischemic Cardiomyocytes by Mitigating Oxidative Stress

1Department of Cardiovascular Medicine, The First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin 150001, China
2Department of Coronary Care Unit, The First Hospital of Harbin, 151 Diduan Street, Daoli District, Harbin 150000, China
3Department of Cardiovascular Medicine, The First People’s Hospital of Luoyang, 88 East Zhongzhou Road, Luoyang 471000, China
4Department of Cardiovascular Medicine, Heilongjiang Province Land Reclamation Headquarters General Hospital, 235 Hashuang Road, Nangang District, Harbin 150088, China

Correspondence should be addressed to Lu Fu; moc.361@aidanuluf

Received 7 June 2017; Accepted 9 August 2017; Published 17 September 2017

Academic Editor: Haifa Qiao

Copyright © 2017 Jing Yang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Oxidative stress participates in numerous myocardial pathophysiological processes and is considered a therapeutic target for myocardial ischemia and heart failure. Guanxintai (GXT), a traditional Chinese medicine, is commonly used to treat cardiovascular disease on account of its numerous beneficial physiological activities, such as dilating coronary arteries, inhibiting platelet aggregation, and reducing the serum lipid content. However, the antioxidative properties of GXT and potential underlying mechanisms remain to be established. In the present study, we investigated the protective effects of GXT on ischemic cardiomyocytes and the associated antioxidative mechanisms, both in vivo and in vitro. Notably, GXT treatment reduced the degree of cardiomyocyte injury, myocardial apoptosis, and fibrosis and partially improved cardiac function after myocardial infarction. Furthermore, GXT suppressed the level of ROS as well as expression of NADPH oxidase (NOX) and phospho-p38 mitogen-activated protein kinase (MAPK) proteins. Our results collectively suggest that the protective effects of GXT on ischemic cardiomyocytes are exerted through its antioxidative activity of NOX inhibition.