Abstract
Cardiovascular disease is the world’s leading cause of death. Lipoxidation plays a relevant role in the onset of cardiovascular diseases (CVD) causing about17 to 19 deaths annually. The usage of traditional drugs was influenced by the need for effective medications for the treatment of cardiovascular disease without side effects. The study aimed at investigating antilipidemic and antioxidative protection offered by Adansonia digitata leaf extract on doxorubicin-induced cardiotoxicity in wistar rats. Thirty male wistar rats were grouped into five of six (6) each:(1) normal control, received 0.5 mL of distilled water (2) received 20 mg/kg of DOX only (3) received 20 mg/kg of DOX +100 mg/kg of A. digitata leaf extract (4) received 20 mg/kg of DOX + 200 mg/kg of A . digitata leaf extract and (5) received 20 mg/kg of DOX+400 mg/kg of A. digitata. DOX was administered subcutaneously weekly while extract was given orally/day for three weeks. Results revealed significant (p>0.05) increased in Troponin T, Creatinekinase and Lactate dehydrogenase in group2 against normal control. Reduction of these parameters was observed across the groups administered A. digitata extract. Elevation of MDA was recorded in group2 compared with normal control. This parameter decreased upon treated with the extract. Significant (p<0.05) reductions in Chol, TG, and LDL levels were obtained in group fed 400 mg/Kg b. wt of the extract in comparison with group 2 (DOX –induced only) and normal control. Significant variations of Chol, TG and LDL levels were observed within the text groups in dose dependent manner. HDL increased in all the text groups except group2.CAT and GPx activities decreased significantly (p>0.05) while SOD activity was non- significantly (p>0.05) decreased. Increase activities of these antioxidant enzymes were recorded across the test groups administered extract against group2 (DOX –induced only) and normal control. In this study A. digitata leaf extract has demonstrated its potential to delaying lipid peroxidation and protects oxidative damage induced by doxorubicin in the experimental rats.
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