Experimental myocardial necrosis in rats: Role of arjunolic acid on platelet aggregation, coagulation and antioxidant status

Citation
M. Sumitra et al., Experimental myocardial necrosis in rats: Role of arjunolic acid on platelet aggregation, coagulation and antioxidant status, MOL C BIOCH, 224(1-2), 2001, pp. 135-142
Citations number
40
Categorie Soggetti
Cell & Developmental Biology
Journal title
MOLECULAR AND CELLULAR BIOCHEMISTRY
ISSN journal
03008177 → ACNP
Volume
224
Issue
1-2
Year of publication
2001
Pages
135 - 142
Database
ISI
SICI code
0300-8177(2001)224:1-2<135:EMNIRR>2.0.ZU;2-M
Abstract
Arjunolic acid, a new triterpene and a potent principle from the bark of Te rminalia arjuna, has been shown to provide significant cardiac protection i n isoproterenol induced myocardial necrosis in rats. To further explore the mechanism of action of arjunolic acid, antiplatelet activity, anticoagulan t assays, electrocardiographic changes, serum marker enzymes, antioxidant s tatus, lipid peroxide and myeloperoxidase (MPO) have been measured and the results are compared with a potent cardioprotective drug, acetyl salicylic acid (ASA). Administration of isoproterenol produces electrocardiographic c hanges such as decreased R amplitude and increased ST segment elevation and has resulted in an increase in serum marker enzyme levels as well as a dec rease in enzymatic and nonenzymatic antioxidant levels. Arjunolic acid at a n effective dosage of 15 mg/kg body weight (pre and post treatment),when ad ministered intraperitoneally (i.p.), effects a decrease in serum enzyme lev els and the electrocardiographic changes get restored towards normalcy. Arj unolic acid treatment is also shown to prevent the decrease in the levels o f superoxide dismutase, catalase, glutathione peroxidase, ceruloplasmin, al pha -tocopherol, reduced glutathione (GSH), ascorbic acid, lipid peroxide, MPO and the cardioprotection is confirmed by the histopathological studies. This study shows that the cardioprotection of arjunolic acid pre and post t reatment could possibly be due to the protective effect against the damage caused by myocardial necrosis.