Title: Therapeutic Benefits of Garlic against Alloxan-Induced Diabetic in Rats
Author: El-Khedr Mohamed Mostafa El-Gamal
DOI: https://dx.doi.org/10.18535/jmscr/v5i2.39
Abstract
Diabetes mellitus is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both. The chronic hyperglycemia of diabetes is associated with long-term damage, dysfunction, and failure of various organs, especially the eyes, kidneys, nerves, heart, and blood vessels. The present study was carried out to investigate the effects of garlic (Allium sativum Linn) juice on biochemical parameters, enzyme activities and lipid peroxidation in alloxan-induced diabetic rats. Alloxan was administered as a single dose (150mg/kgBW) to induce diabetes. A dose of 1ml of garlic juice/100g body weight (equivalent to 0.4 g/100g BW) was orally administered daily to alloxan-diabetic rats for four weeks. The levels of glucose, urea, creatinine and bilirubin were significantly (p < 0.05) increased in plasma of alloxan-diabetic rats compared to the control group. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and alkaline and acid phosphatases (AlP, AcP) activities were significantly (p < 0.05) increased in plasma and testes of alloxan-diabetic rats, while these activities were decreased in liver compared with the control group. Brain LDH was significantly (p < 0.05) increased. The concentration of thiobarbituric acid reactive substances and the activity of glutathione S-transferase in plasma, liver, testes, brain, and kidney were increased in alloxan diabetic rats. Treatment of the diabetic rats with repeated doses of garlic juice could restore the changes of the above parameters to their normal levels. The current results showed that garlic juice exerted antioxidant and antihyperglycemic effects and consequently may alleviate liver and renal damage caused by alloxan-induced diabetes.
Keywords: Rats; Alloxan; Garlic; Biochemical parameters; Enzymes; Lipid peroxidation.
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