Abstract
Introduction:
Hypercholesterolemia and oxidative stress are risk factors of cardiovascular diseases.
Objectives:
This study investigated the hypolipidemic effect of cocoa powder extract (CPE) in an experimental model of hypercholesterolemia, using Questran as a reference.
Methods:
Hypercholesterolemia in rats was induced by oral administration of 30 mg/kg cholesterol for eight weeks. Three groups concurrently received Questran (0.26 g/kgb) and CPE (100 mg/kg and 200 mg/kg) respectively. Hypercholesterolemia and dyslipidemia were assessed by lipid profile. Reduced glutathione (GSH), Superoxide dismutase (SOD), Catalase (CAT), Glutathione-S-transferase (GST) and malondialdehyde (MDA) level were also assessed to evaluate the antioxidant status of rats.
Results:
There was 56% and 97% increase in total and LDL-cholesterol and 59% decrease in HDL-cholesterol levels on cholesterol administration. Concurrent administration of CPE (100 mg/kg) significantly (p < 0.05) decreased total cholesterol (19%) and LDL-cholesterol (22%) and increased HDL-cholesterol (286%) levels while at 200 mg/kg, 55% and 64% reductions in total and LDL-cholesterol and 250% increase in HDL-cholesterol levels were observed. No significant changes were observed in phospholipid levels. Body weights of rats were not significantly different among groups and CPE (100 mg/kg) ameliorated the cholesterol-induced enlargement of the liver and heart by 14% and 15% respectively and at 200 mg/kg by 21% in the heart. GSH and CAT were significantly depleted, and MDA and SOD significantly elevated in liver and heart of Cholesterol-fed rats. No significant changes in GST, alanine and aspartate aminotransferases occurred among groups. CPE treatment modulated these changes.
Conclusion:
Cocoa powder possesses hypolipidemic potential and may be relevant in treating pathologies with dyslipidemia as an underlying cause.
