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Toxicol Mech Methods. 2007;17(1):57-65. doi: 10.1080/15376510600822649.

Protective effect of ursolic Acid against myocardial ischemia induced by isoproterenol in rats.

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Department of Biochemistry, Faculty of Science, Annamalai University, Annamalai nagar, 608 002, Tamil Nadu, India.


Sustained high levels of circulating catecholamines may induce cardiotoxicity through oxidative mechanisms. Isoproterenol is a synthetic catecholamine with increasing attention owing to this application in cardiology. The aim of the present study was to investigate the cardioprotective effects of ursolic acid against isoproterenol-induced myocardial ischemia. Normal Wistar strain rats were pretreated with UA (20, 40, and 60 mg/kg, s.c.) for 7 days and then intoxicated with isoproterenol (ISO, 85 mg/kg, s.c. for 2 consecutive days). Hearts were excised from the experimental animals and assessed for the activities of cardiac markers [alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and creatine phosphokinase (CPK)], the levels of lipid peroxide products [thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (HPs), and conjugated dienes (CDs)], myeloperoxidase (MPO), lipid profiles [total cholesterol (TC), free cholesterol, ester cholesterol, triglycerides (TG), free fatty acids (FFAs), and phospholipids (PLs)], and membrane-bound enzymes (total ATPase, Na(+)K(+)ATPase, Ca(2+)ATPase, and Mg(2+)ATPase). In ISO-treated group, shrinkage of cardiac markers and elevated lipid peroxidation with compromised lipid profiles in the heart where accompanied by the decreased activities of membrane-bound enzymes. The prior administration of UA significantly (p < 0.05) prevented the isoproterenol-induced alterations and restored the enzymes to near normal. These findings indicate the cardioprotective activities of UA during isoproterenol-induced myocardial ischemia.


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