Cardioprotective Effects of Virgin Coconut Oil and Carvedilol Against Doxorubicin-induced Cardiotoxicity in Male Mice: Biochemical and Histopathological Evaluation

Abstract

Background: Doxorubicin (DOX) is a potent chemotherapeutic agent with a broad spectrum of anticancer activity. However, its clinical utility is limited by its propensity to induce cardiotoxicity, characterized by oxidative stress and myocardial degeneration. Objective: This study aimed to evaluate the cardioprotective effects of virgin coconut oil (VCO) and carvedilol (CARV) against DOX-induced Cardiotoxicity in mice, using biochemical and histopathological Parameters. Methods: Thirty-two adult mice were randomly assigned to four groups: control, DOX-only (3.75 mg/kg/week, i.p.), DOX+VCO (5 ml/kg/day, orally), and DOX+CARV (5 mg/kg, orally, thrice weekly) for 28 days. At the end of treatment, heart tissues were analyzed for malondialdehyde (MDA) and superoxide dismutase (SOD) levels, and examined histologically. Results: The DOX only group showed a significant increase in malondialdehyde (MDA) levels indicating oxidative cardiac damage. The DOX + CARV group had significantly decreased MDA levels, whereas the DOX + VCO group exhibited a mild, non-significant decrease. SOD levels decreased further in both DOX + CARV and DOX + VCO groups. Histopathological analysis revealed severe cardiac damage in the DOX group, which was markedly attenuated in the DOX + CARV group and moderately reduced in the DOX + VCO group. Conclusion: Virgin coconut oil and carvedilol conferred notable histological protection against doxorubicin-induced cardiac injury, preserving myocardial structure and function. Despite limited antioxidant effects biochemically, their cardioprotective potential may involve alternative mechanisms beyond enzymatic restoration, including non-enzymatic scavenging and anti-inflammatory pathways. These findings underscore the complexity of redox regulation in cardiotoxicity and support further exploration of combination therapies and time-dependent antioxidant responses.