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

2026

Closed access Metadata (CSL-JSON)
DOI 10.1080/08923973.2026.2635988
Data confidence 70 medium
How this score is calculated

It is built from checkable properties of the record itself: whether the article has a DOI, how many independent sources confirmed its data, whether the required fields are filled in, and how recent the latest confirmation is. Disagreement between sources and a missing identifier lower it. A value of 80 or above means the record was published without further checking; 60 to 79 means it is published at reduced confidence, with a manual check advisable. A record verified by an editor by hand is never pushed below 90 by a recalculation. This scores our data about the article, not the article itself.

Abstract

OBJECTIVE: 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. METHODS: = 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. RESULTS: 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. CONCLUSIONS: 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.