Objective. Diabetic nephropathy is the most commonly seen cause of chronic renal failure, and oxidative stress is important in etiology. In the present study, favorable effects (if any) of the treatment with a thiazolidinedione group drug, pioglitazone, on antioxidant enzyme levels in the renal tissue, renal histopathology, and inflammatory cytokine levels have been investigated. Method. Forty male Wistar rats were divided into 4 groups as the control, diabetic control, and 10 and 30？mg pioglitazone-administered diabetic groups. After 4 weeks, antioxidant enzyme levels in renal tissues and inflammatory markers were investigated. Results. Blood glucose levels did not differ between the diabetic control and drug-administered groups. In pioglitazone-administered rats, histopathological findings such as tubular dilation, necrotic tubular epithelium, glomerular focal necrosis, and vascular consolidation were observed at a lesser extent than the diabetic control group. Any difference was not detected between the diabetic groups with respect to the levels of malondialdehyde, superoxide dismutase, catalase, glutathione, nitric oxide, interleukin-6, and tumor necrosis factor-alpha. Conclusion. Pioglitazone regressed development of histopathological lesions such as glomerular focal necrosis, tubular epithelial necrosis, tubular dilation, and vascular wall consolidation. However, any favorable effect on antioxidant enzyme levels in renal tissues and inflammation markers was not detected. 1. Introduction Diabetes mellitus has become the most frequently seen global etiological factor for the end-stage renal failure. According to the data published by World Health Organization, in the year 2030, the number of diabetics was predicted to amount to 370 million patients [1]. As proved in many investigations, strict glycemic and heart rate control prevent occurrence and progression of diabetic nephropathy [2–4]. However, especially in some of the type 2 DM patients, complications already develop at the time of diagnosis, and strict glycemic control cannot be always achieved. Therefore, development of treatment modalities preventing occurrence or progression of diabetic nephropathy seems to be an urgent need. Pathophysiological mechanisms contributing to the formation of diabetic nephropathy and treatment modalities directing to that end have been investigated. Increased activation of polyol, protein kinase c and hexosamine pathways, and intracellular AGEs (advanced glycation end products) were determined as basic mechanisms of hyperglycemic tissue damage [5]. Oxidative
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