Boswellia serrata Resin Mitigates Doxorubicin-Induced Cardiac Oxidative Stress, Biomarker Leakage, and Myocardial Histopathological Injury in Rats
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Abstract
Doxorubicin is a potent antineoplastic agent, but its clinical use is limited by dose-dependent cardiotoxicity. The resin of Boswellia serrata has antioxidant and anti-inflammatory properties and may confer cardio protection. The present study was planned to assess the protective effect of Boswellia serrata resin extract (BSE) on doxorubicin induced cardiac injury in rats. Adult male Wistar rats were divided into six groups (n = 48); control, BSE only, doxorubicin (DOX), DOX + BSE 250 mg/kg, DOX + BSE 500 mg/kg, and DOX + carvedilol. BSE was administered orally, and doxorubicin was administered intraperitoneally to induce cardiotoxicity. Serum CK-MB, LDH, cardiac troponin-I and AST were estimated. Myocardial MDA, GSH, SOD, CAT and GPx were determined. Cardiac histopathology was assessed semi-quantitatively. Doxorubicin markedly reduced body weight gain, elevated heart weight indices and serum cardiac injury biomarkers, myocardial MDA and reduced GSH and antioxidant enzyme activities. Histopathological signs of DOX included degeneration of myocardial fibres, sarcoplasmic vacuolation, fragmentation of myofibrils, inflammatory infiltration, vascular congestion, haemorrhage and necrosis. Co-treatment with BSE significantly attenuated these biochemical and histological alterations, and the protection was greater at 500 mg/kg than at 250 mg/kg. To summarize, attenuation of doxorubicin-induced cardiotoxicity by BSE was associated with reduction in cardiac injury biomarkers and lipid peroxidation, enhancement of antioxidant defences and preservation of myocardial architecture, supporting a potential cardioprotective effect of BSE, which may be related mainly to mitigation of oxidative and structural myocardial injury.
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