Abstract
Background: Diabetes causes increased oxidative stress, to play an important role in the pathogenesis of various diabetic complications. The present study investigated the protective potential of allicin against diabetes in rat model. Methodology: Animals were injected a single dose of streptozotocin (55mg/kg.b.wt) to induce diabetes. Control and diabetic rats were treated with allicin (20 mg/kg.b.wt) for 30 days. Glibenclamide (10mg/kg.b.wt) was used as a positive control. After the experimental regimen, the rats were sacrificed and the blood was collected and serum was separated. Blood sugar, body weight, total protein, oxidative stress markers (TBARS, CAT, SOD and GSH) and inflammatory markers (TNF-α and IL-6) were used to bio-monitor the protective potential of allicin. Results: The experimental animals lost weight significantly, exhibited elevated blood sugar levels, decreased protein levels (p<0.05) in comparison to control animals; these alteration were corrected after allicin therapy. The significant elevation of TBARS content, reduction in total glutathione content and declined CAT and SOD activities in experimental animals; which were normalized following allicin therapy. The altered serum inflammatory markers were significantly reduced to near normal levels. No significant alterations in allicin alone administered rats. Conclusion: We thus conclude that allicin has potent antihyperglycemic, anti-lipidperoxidative and anti- inflammatory potential in diabetic animals.
Highlights
Diabetes is a common life-long health condition caused by an absolute or relative lack of insulin and is characterized by hyperglycemia in the postprandial and fasting state
The experimental animals lost weight significantly, exhibited elevated blood sugar levels, decreased protein levels (p
Body weights were similar in all the groups at baseline
Summary
Diabetes is a common life-long health condition caused by an absolute or relative lack of insulin and is characterized by hyperglycemia in the postprandial and fasting state. The number of people with type I and type II diabetes are dramatically increasing on a global scale (Leila, et al 2007). The World Health Organization (WHO) estimates that more than 180 million people in the world have diabetes and that this number will double by 2030 (WHO, 2009). Various hypotheses to explain the genesis of free radicals in diabetes include autoxidation processes of glucose, the non-enzymatic and progressive glycation of proteins with the increased formation of glucose-derived advanced glycosylation end products (AGEs), and enhanced glucose flux through the polyol pathway (Tiwari and Rao, 2002). Diabetes causes increased oxidative stress, to play an important role in the pathogenesis of various diabetic complications. The present study investigated the protective potential of allicin against diabetes in rat model
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