Examination of the effect of riboflavin on TNF-α, Cas-3 and SIRT1/p53/Bax/Bcl-2 gene expression in diatrizoate-induced experimental nephropathy model

Organs or tissues must be surrounded by a substance of different densities to be visualized radiographically. Organs or tissues that are indistinguishable from other structures can be made visible by increasing the contrast ratios of themselves or their surroundings. Diatrizoate is among the iodinated contrast agents with high osmolality and ionic monomer structure. Due to its properties, it may cause an increase in oxidative stress and trigger inflammation and apoptosis processes following its use. Riboflavin is an antioxidant nutrient that can have an antioxidant effect, heal DNA damage, and regulate urea and creatinine levels. This study aimed to examine the impact of riboflavin on TNF-α, Cas-3, and SIRT1/p53/Bax/Bcl-2 gene expressions in the diatrizoate-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, RCM (Day 3, intraperitoneal 10 ml/kg and 2.5-3 ml of Urografine in a single dose), RCM + Riboflavin (Day 3, 100 mg/kg Riboflavin by oral gavage; Day 3, intraperitoneal 10 ml/kg and 2.5-3 ml of Urografine in a single dose) and Riboflavin (3 days, 100 mg/kg Riboflavin by oral gavage). All rats were subjected to water restriction 24 hours before the administration of the radiocontrast agent. 24 hours after the administration of the radiocontrast agent, euthanasia was performed by surgical exsanguination following abdominal incision. Histopathological, immunohistochemical (TNF-α and Cas-3), biochemical (TAS, TOS, OSI, Urea, and Creatinine), and genetic (SIRT1, p53, Bax, and Bcl-2) analyses were performed on the kidney tissues. In the RCM group, pathologic changes, immunohistochemical TNF-α and Cas-3 expressions, biochemical TOS, OSI, urea, and creatinine levels, genetic p53, and Bax expressions increased, while biochemical TAS levels, genetic SIRT1 and Bcl-2 expressions decreased. It was determined that these findings observed in the RCM group were reversed with riboflavin treatment. All these results suggest that iodinated contrast media-induced renal damage develops through oxidative stress, inflammation, and apoptosis mechanisms and that "Riboflavin" administration can protect renal function by suppressing these processes.