Cardioprotective effect of lipistat against doxorubicin induced myocardial toxicity in albino rats

Preventive role of lipistat against doxorubicin induced myocardial toxicity in rats has been reported. Cardiotoxicity was produced by doxorubicin administration (15 mg/kg for 2 weeks). Lipistat (350 mg/kg, orally) was administered as pretreatment for 2 weeks and then for 2 weeks alternated with doxo...

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Veröffentlicht in:Indian journal of experimental biology 2009-01, Vol.47 (1), p.41
Hauptverfasser: Koti, B C, Vishwanathswamy, A H M, Wagawade, Jyoti, Thippeswamy, A H M
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Sprache:eng
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Zusammenfassung:Preventive role of lipistat against doxorubicin induced myocardial toxicity in rats has been reported. Cardiotoxicity was produced by doxorubicin administration (15 mg/kg for 2 weeks). Lipistat (350 mg/kg, orally) was administered as pretreatment for 2 weeks and then for 2 weeks alternated with doxorubicin. The general observations, mortality, histopathology, biomarker enzymes like lactate dehydrogenase (LDH) and creatine phosphokinase (CPK), serum lipid profiles like total cholesterol, triglycerides, low-density lipoprotein (LDL) and high-density lipoprotein (HDL), antioxidant enzymes such as glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) were monitored after 3 weeks of last dose. Pretreatment with the lipistat significantly protected myocardium from the toxic effects of doxorubicin by reducing the elevated level of biomarker enzymes like LDH and CPK to the normal and serum lipids such as total cholesterol, triglyceride and LDL back to normal. Lipistat increases the decreased level of GSH, SOD and CAT and decreases the increased level of malondialdehyde in cardiac tissue. The repeated administration of doxorubicin causes cardiomyopathy associated with an antioxidant deficit and increased level of lipid profiles by interfering with fatty acid metabolism. The results support the lipid lowering and antioxidant properties of lipistat, which indicate the cardioprotective property against doxorubicin induced cardiotoxicity.
ISSN:0019-5189