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Cardioprotective effects and underlying mechanisms of oxymatrine against Ischemic myocardial injuries of rats
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AbstractOxymatrine 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 ischemia, 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 © 2008 John Wiley & Sons, Ltd.
Title: Cardioprotective effects and underlying mechanisms of oxymatrine against Ischemic myocardial injuries of rats
Description:
AbstractOxymatrine 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 ischemia, 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 © 2008 John Wiley & Sons, Ltd.
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