It is believed that adipose tissue-derived molecules contribute to systemic insulin resistance and to the pathogenesis of most of the metabolic complications of type 2 diabetes mellitus, atherosclerosis, and obesity. Type 2 diabetes (T2DM) plays a causative role in the pathogenesis of atherosclerosis. Diabetes is considered to be a very important factor in promoting low density lipoprotein (LDL) oxidation. Stimulation of lipid peroxidation in LDLs during diabetes is associated with strong oxidation of cholesterol and glucose during oxidative and carbonyl stress, respectively. These data describe the relationship between hyperglycemia and atherosclerosis in diabetic patients. Many studies have shown that inflammation plays a very important role in the pathogenesis of T2DM. Inflammatory mechanisms and cytokine production activated by stress via the inflammasome may further alter the normal structure of β-cells by inducing pancreatic islet cell apoptosis. The aim of this study was to determine the effects of acetylsalicylic acid (ASA) on inflammation, oxidative stress and serum protein concentrations in rats with experimentally induced T2DM. For the study, male wistar rats were used. Obesity was established by body weight gain at a 5% level and insulin resistance was determined in the rats fed with a high-fat diet. T2DM was induced by a streptozotocin injection in obese rats. ASA at a dose of 150 mg/kg b.w. was given orally once daily for five weeks. The levels of pro-inflammatory cytokines (in both serum and brain homogenate), total antioxidant status (TAS), total oxidant status (TOS), and c-reactive protein (CRP) (in the serum) were analysed at the end of the treatment. Serum proteins were also analysed by electrophoresis. Although TNF-α was increased in the blood, ASA treatments did not effect the levels of cytokines in the blood and brain tissue of diabetic rats. Induction of diabetes increased both total antioxidant status and total oxidant status in the blood. ASA treatment also increased blood total antioxidant status of diabetics. Levels of serum proteins, especially albumin, were affected by diabetes and ASA treatments. These results indicated that diabetes induced inflammation and oxidative stress. It may be said that ASA treatment at a dose of 150 mg/kg b.w. for five weeks is not sufficient for amelioration of the inflammation induced by diabetes. This study confirmed that ASA has antioxidant effects. Further studies are needed to investigate the role of ASA in pro-inflammatory immuno-modulation in diabetes.
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