Abstract
Purpose. In this study, we tested the hypothesis that rosiglitazone (RSG) with insulin is able to quench oxidative stress initiated by high glucose through prevention of NAD(P)H oxidase activation. Methods and Materials. Male albino Wistar rats were randomly divided into an untreated control group (C), a diabetic group (D) that was treated with a single intraperitoneal injection of streptozotocin (45 mgkg−1), and rosiglitazone group that was treated with RSG twice daily by gavage and insulin once daily by subcutaneous injection (group B). HbA1c and blood glucose levels in the circulation and malondialdehyde and 3-nitrotyrosine levels in left ventricular muscle were measured. Result. Treatment of D rats with group B resulted in a time-dependent decrease in blood glucose. We found that the lipid profile and HbA1c levels in group B reached the control group D rat values at the end of the treatment period. There was an increase in 3-nitrotyrosine levels in group D compared to group C. Malondialdehyde and 3-nitrotyrosine levels were found to be decreased in group B compared to group D (P < 0.05). Conclusion. Our data suggests that the treatment of diabetic rats with group B for 8 weeks may decrease the oxidative/nitrosative stress in left ventricular tissue of rats. Thus, in diabetes-related vascular diseases, group B treatment may be cardioprotective.
Highlights
Hyperglycemia induces protein glycation, systemic low grade inflammation, and endothelial dysfunction [1]
Treatment of insulin and rosiglitazone may decrease oxidative stress in diabetic rats, which may be cardioprotective in setting diabetic vascular disease, the aim of the present study was to dissect the molecular mechanisms underlying the effects of RSG on hyperglycemia-induced reactive oxygen species (ROS) production
TAG: triacylglycerol, TC: total cholesterol, HDL-C: high-density lipoprotein-cholesterol, very low density lipoprotein-cholesterol (VLDL-C): very lowdensity lipoprotein-cholesterol, low density lipoprotein-cholesterol (LDL-C): low-density lipoprotein-cholesterol levels of study groups are shown in Figures 1 and 2
Summary
Hyperglycemia induces protein glycation, systemic low grade inflammation, and endothelial dysfunction [1]. Diabetes is one of the main risk factor for cardiovascular disease. Hyperglycemia-induced endothelial dysfunction is characterized by an enhanced production of reactive oxygen species (ROS), which are important actors in the development of vascular damage. Antioxidant agents are able to rescue hyperglycemia-induced vascular dysfunction [1, 2]. Insulin resistance is a fundamental abnormality in the pathogenesis of type-2 diabetes. A number of different mechanisms have been proposed to explain the mechanism of insulin resistance. Recent information suggests that a common feature of the development of insulin resistance is an increased production of ROS and that reduction in ROS production results in improved insulin sensitivity [3]
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