To investigate whether aminoguanidine ameliorates streptozotocin-induced renal oxidative stress and inflammation in diabetic mice. Diabetic nephropathy is characterized by structural and functional changes in both glomerular, tubular and finally impairment of renal function. Streptozotocin [100mg/kg body weight dissolved in freshly prepared citrate buffer and administered through tail vein injection] was used to induce diabetes in male Swiss albino male mice and received standard diet throughout study period [8weeks]. Diabetic mice group received aminoguanidine [100mg/kg/day]. We studied streptozotocin-induced renal changes by noticing body weight, kidney weight and their ratio, histological and electron microscopic studies. Antioxidant activities like glutathione, superoxide dismutase and catalase were analyzed. RT-PCR gene expression studies were used to analyze the inhibitory effect of aminoguanidine against diabetes-induced IL-1β, IL-6 and TNF-α. STZ-diabetic mice showed significantly increased oxidative stress indices like melonaldehyde and nitric oxide levels, reduced endogenous antioxidant enzyme activities, whereas aminoguanidine treatment normalizes these pathological changes and may play a crucial role in oxidative stress-related changes during STZ-induced diabetic mice. Aminoguanidine treatment restored diabetes-induced structural and biochemical alterations. RT-PCR gene expression studies suggests that aminoguanidine protect STZ-induced renal pathological changes probably by attenuating diabetes-induced IL-1β, IL-6 and TNF-α gene expression.