Hypoglycemic, Hematologic and Hypolipidemic Activity of Mucuna Pruriens Ethanol Leaf Extract in Alloxan Induced Diabetic Rats

Abstract

Aim: This study investigated the hypoglycemic, hematologic and hypolipidemic potentials of Mucuna pruriens ethanol leaf extract (MELE) in alloxan induced diabetic rats. Study Design: Experimental Animal Model. The study was conducted in the Physiology Laboratory of the Department of Veterinary Physiology and Pharmacology, Michael Okpara University of Agriculture, Umudike, Nigeria between November, 2013 and February, 2014. Methodology: Diabetic rats were divided into 4 groups of 7 animals each (groups 2-5). Group1 comprising of 7 normal rats received 0.2ml normal saline and served as the normal control group. Group 2 received no treatment and served as the diabetic control group. Group 3 was treated with a reference drug, Glibenclamide (5mg/kg) while groups 4 and 5 received 150 and 300mg/kg of MELE respectively. All treatments were done via the oral route and lasted for 21 days. Results: Alldoses of MELE significantly (P<.05) lowered glucose levels in the diabetic rats with 300mg/kg lowering blood glucose from 311.80 ± 37.10 in diabetic rats to 91.30 ± 2.26 by the end of 21 days. The hypoglycemic effect of MELE compared favorably with that of Glibenclamide. Red blood cells (RBC) counts, packed cell volume (PCV),hemoglobin values were all significantly raised (P<.05) in treated rats, while the increased WBC value in diabetic rats was lowered. The levels of total cholesterol, triglycerides, low density lipoprotein cholesterol (LDL-C) and very low density lipoprotein cholesterol (VLDL-C) were significantly (P<.05) decreased in the diabetic treated rats with increase in the levels of high density lipoprotein cholesterol (HDL-C). Conclusion: These results suggest that MELE contain active principles with hypoglycemic, hematologic and hypolipidemic properties and could be valuable in managing diabetic mellitus and correcting the hematological and lipid profile abnormalities associated with the pathophysiology of the disease.