Abstract

Hyperglycemia-induced increase in oxidative stress is implicated in diabetic complications. This study investigated the effect of metformin and/or glibenclamide in combination with honey on antioxidant enzymes and oxidative stress markers in the kidneys of streptozotocin (60 mg/kg; intraperitoneal)-induced diabetic rats. Diabetic rats were randomized into eight groups of five to seven rats and received distilled water (0.5 mL); honey (1.0 g/kg); metformin (100 mg/kg); metformin (100 mg/kg) and honey (1.0 g/kg); glibenclamide (0.6 mg/kg); glibenclamide (0.6 mg/kg) and honey (1.0 g/kg); metformin (100 mg/kg) and glibenclamide (0.6 mg/kg); or metformin (100 mg/kg), glibenclamide (0.6 mg/kg) and honey (1.0 g/kg) orally once daily for four weeks. Malondialdehyde (MDA) levels, glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities were significantly elevated while catalase (CAT) activity, total antioxidant status (TAS), reduced glutathione (GSH), and GSH:oxidized glutathione (GSSG) ratio was significantly reduced in the diabetic kidneys. CAT, glutathione reductase (GR), TAS, and GSH remained significantly reduced in the diabetic rats treated with metformin and/or glibenclamide. In contrast, metformin or glibenclamide combined with honey significantly increased CAT, GR, TAS, and GSH. These results suggest that combination of honey with metformin or glibenclamide might offer additional antioxidant effect to these drugs. This might reduce oxidative stress-mediated damage in diabetic kidneys.

Highlights

  • Diabetes mellitus is one of the five main causes of death in the world [1]

  • Treatment of diabetic rats with metformin or glibenclamide did not produce any significant effects on CAT and glutathione reductase (GR) activities compared to diabetic control rats

  • Metformin or glibenclamide combined with honey showed significantly (p < 0.05) increased CAT and GR activities in diabetic rats compared to the diabetic control rats

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Summary

Introduction

Diabetes mellitus is one of the five main causes of death in the world [1]. The most common form of diabetes, which accounts for 90–95% of all diabetic cases, is type 2 diabetes [2]. It is a metabolic disorder characterized by hyperglycemia as a result of insulin resistance. The global prevalence of diabetes mellitus was estimated as 171 million people in 2000 and this figure is predicted to increase to 366 million by 2030 [3]. Since diabetes mellitus is a heterogeneous disorder with multiple causes, the beneficial effects of combined therapeutic agents aimed at specific patho-biological pathways of diabetes and its complications have been reported [4,5]

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