Streptozotosin ile Diyabet Oluşturulmuş Ratlarda L-Arjinin’in Dönüştürücü Büyüme Faktör Beta 1 (TGF-β1) Ekspresyonu ve Erken Böbrek Değişiklikleri Üzerine Etkileri

Diabetic nephropathy (DN) is a prevalent microvascular complication of diabetes mellitus, occurring in more than 40% of affected individuals, with reactive oxygen species–induced endothelial dysfunction playing a central role in its development. L-arginine may exert protective effects by interacting with these oxygen metabolites. This study investigated the effects of L-arginine on early renal changes in streptozotocin-induced diabetic rats. Additionally, renal levels and localization of transforming growth factor beta 1 (TGF-β1), an important fibrogenic factor involved in DN and endothelial-mesenchymal transition, were evaluated by ELISA and immunohistochemistry. Forty-eight male Wistar albino rats (250-300 g) were divided into four groups (n=12); control (0.1 mol/L sodium citrate buffer i.p.); L-arginine (100 mg/kg by gavage); STZ (50 mg/kg, i.p.); STZ+L-arginine (50 mg/kg STZ i.p.+ 100 mg/kg L-arginine by gavage). STZ was administered as a single dose, and L-arginine was given for twenty-one days. Histopathological examination of diabetic kidneys revealed glomerular enlargement, erythrocyte congestion in glomerular and interstitial vessels, cytoplasmic vacuolization in tubular epithelium, and hyaline deposition in glomeruli and tubules. TGF-β1 expression was detected in proximal and distal tubular epithelial cells and in the vascular media of all groups. However, TGF-β1 immunoreactivity was very mild in the control and L-arginine groups compared with the diabetes-induced groups. ELISA results confirmed significantly elevated renal TGF-β1 levels in diabetic rats, while L-arginine administration markedly reduced these increases. In conclusion, diabetes induced notable morphologic kidney alterations accompanied by increased TGF-β1 levels. L-arginine treatment attenuated TGF-β1 elevation, suggesting potential protective effects against diabetes-related renal vascular damage.