Cardioprotective effects and underlying mechanisms of oxymatrine against ischemic myocardial injuries of rats

被引:95
作者
Hong-li, Sun [1 ,2 ]
Lei, Li [3 ]
Lei, Shang [1 ]
Dan, Zhao [4 ]
De-li, Dong [1 ]
Guo-fen, Qiao [1 ]
Yan, Liu [1 ]
Wen-feng, Chu [1 ]
Bao-feng, Yang [1 ]
机构
[1] Harbin Med Univ, Dept Pharmacol, Biopharmaceut Engn Key Lab Heilongjiang Prov Incu, State Key Lab, Harbin 150081, Peoples R China
[2] Harbin Med Univ, Dept Pharmacol, Daqing 163319, Peoples R China
[3] Harbin Med Univ, Clin Coll 5, Dept Surg, Daqing 163316, Peoples R China
[4] Harbin Med Univ, Dept Nutr & Food Hyg, Harbin 150081, Peoples R China
关键词
oxymatrine; myocardial infarction; apoptosis; Bcl-2; Fas; intracellular Ca2+;
D O I
10.1002/ptr.2452
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Oxymatrine has been demonstrated to have a variety of pharmacological actions. Accumulating evidence indicates that oxymatrine may exert a protective effect on the cardiovascular system. The study was designed to explore the possible role of oxymatrine against myocardial ischemic damage and several related signaling pathways as potential mechanisms. The protective properties of oxymatrine were studied in a rat model of acute myocardial infarction due to permanent ligation of the left anterior descending coronary artery. The results showed that administration of oxymatrine relieved myocardial injuries during ischernia, and this was achieved by protecting cardiomyocytes from apoptotic death. The beneficial effects of oxymatrine were likely mediated by an inhibition of lipid peroxidation (MDA production) and an increase in endogenous antioxidant activity (SOD), activation of the survival signaling molecule (Bcl-2), and a reduction of apoptotic mediator (Fas) and intracellular Ca2+ overload. Copyright (c) 2008 John Wiley & Sons, Ltd.
引用
收藏
页码:985 / 989
页数:5
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