Cardioprotective Effects of Virgin Coconut Oil and Carvedilol Against Doxorubicin-induced Cardiotoxicity in Male Mice: Biochemical and Histopathological Evaluation
Izuchukwu Prince Nweke *
Department of Human Physiology, Alex Ekwueme Federal University, Ndufu-Alike, Ikwo, Ebonyi State, Nigeria.
Cletus Okechukwu Ogadah
Department of Biochemistry, Alex Ekwueme Federal University Ndufu-Alike, Ikwo, Ebonyi State, Nigeria.
Chibuike Victor Chukwu
Department of Epidemiology and Evidence Based Medicine, First Moscow State Medical University Named after I.M Sechenov, Russia.
Dibor Micheal Chukwuebuka
Department of Human Physiology, Alex Ekwueme Federal University, Ndufu-Alike, Ikwo, Ebonyi State, Nigeria.
*Author to whom correspondence should be addressed.
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.
Keywords: Doxorubicin, cardiotoxicity, virgin coconut oil, carvedilol, oxidative stress