Examination of the Effect of Riboflavin on TNF-α, Cas-3 Expression and SIRT1/p53/Bax/Bcl-2 Gene Expression in Diatrizoate-Induced Experimental Nephropathy Model

This study aimed to examine the impact of riboflavin (RF) on tumor necrosis factor-alpha (TNF-α), caspase-3 (Cas-3) expression, and Sirtuin1 (SIRT1)/protein 53 (p53)/Bcl-2-associated X protein (Bax)/B-cell lymphoma gene-2 (Bcl-2) gene expressions in the diatrizoate (DTZ)-induced experimental nephropathy model. Within the scope of the study, 32 Wistar Albino-type female rats were divided into 4 groups (n = 8). The groups were as follows: Control, DTZ (Rats were given 1 ml saline (SF) by oral gavage for three days. On the third day, intraperitoneal 10 ml/kg and 2.5-3 ml in volume of Urografin in a single dose), DTZ + RF (Rats were given 100 mg/kg RF by oral gavage for three days. On the third day, intraperitoneal 10 ml/kg and 2.5-3 ml of Urografin in a single dose) and RF (Rats were given 100 mg/kg RF by oral gavage for three days. On the third day, intraperitoneal 2.5-3 ml of SF in a single dose). Histopathological, immunohistochemical (TNF-α, Cas-3), biochemical (total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), urea and creatinine), and genetic (SIRT1, p53, Bax, Bcl-2) analyses were performed on the kidney tissues. In the DTZ group, pathologic changes, TNF-α and Cas-3 expressions, TOS, OSI, urea, and creatinine levels, p53, and Bax gene expressions increased, while biochemical TAS levels, genetic SIRT1 and Bcl-2 gene expressions decreased. It was determined that these findings observed in the DTZ group were reversed with RF treatment. All these results suggest that DTZ-induced renal damage develops through oxidative stress, inflammation, and apoptosis mechanisms and that RF administration can protect renal function by suppressing these processes.