Protective effects of dexpanthenol against diatrizoate-induced contrast nephropathy via the SIRT1-p53-Bcl-2/Bax pathway in rats.

Contrast agents are widely used in medical imaging to improve tissue differentiation, but they can cause serious inflammatory responses, including contrast-induced nephropathy (CIN). Dexpanthenol (DEX) is known for its antioxidant, anti-inflammatory, and anti-apoptotic properties. This study aimed to investigate the potential protective effects of dexpanthenol in a rat model of diatrizoate-induced CIN. In this study, 32 Wistar albino rats were randomly divided into four groups: control, Urografin (URO; 10 mL/kg, intraperitoneal [i.p.]), URO + DEX (500 mg/kg, i.p. for 3 days), and DEX alone. Renal function markers (serum urea and creatinine), total oxidant status (TOS), total antioxidant status (TAS), and oxidative stress index (OSI) were measured. Histopathological evaluation and immunohistochemical analysis of tumor necrosis factor-alpha (TNF-α) and caspase-3 (Cas-3) were performed. Additionally, SIRT1, Bcl-2, Bax, and p53 mRNA expression levels were assessed. URO administration increased TOS and OSI values and caused significant renal histopathological damage. TNF-α and Cas-3 immunoreactivity, along with Bax and p53 gene expression, were significantly elevated, while Bcl-2 and SIRT1 expression was suppressed. DEX treatment provided partial improvement in these changes, contributed to the preservation of renal architecture, and was associated with improvements in biochemical and molecular parameters approaching those of the control levels. In conclusion, DEX may exert nephroprotective effects against CIN by reducing oxidative stress, inhibiting pro-inflammatory and apoptotic pathways, and increasing anti-apoptotic gene expression. These findings provide a preclinical basis supporting the idea that dexpanthenol is a promising candidate for further translational and clinical studies in contrast-induced renal injury.