Taxifolin attenuates cisplatin-induced kidney damage in rats via suppressing p53 and iNOS

Authors : Gökhan Akçakavak, Özhan Karataş, Zeynep Çelik, Ayşenur Tural, Osman Dağar, Ahmed Abduljabbar, Bahadır Kılınç, Mehmet Tuzcu

Pages : 1-7

Doi:10.35864/evmd.1458328

View : 206 | Download : 147

Publication Date : 2024-07-04

Article Type : Research Paper

Abstract :Cisplatin (CP) is a platinum-based anticancer drug used to treat many different solid tumors. Although CP has strong anticancer properties, its clinical use is limited due to side effects such as ototoxicity, neurotoxicity, myelosuppression and nephrotoxicity. Taxifolin (Tax) is reported to exhibit various possess effects such as anti-inflammatory, antioxidant, antimicrobial, antiviral and anticancer. In this study, we aimed to investigate the possible effects of Tax on CP-induced nephrotoxicity. This study consisted of Control (C), Taxifolin (Tax), Cisplatin (CP) and Cisplatin + Taxifolin (CP + Tax) groups, and there were 6 rats in each group. CP was administered to rats intraperitoneally (i.p.) in a single dose of 7 mg/kg, and Tax was administered orally at a dose of 50 mg/kg for 7 consecutive days. Histopathologically, significant changes such as tubular epithelial degeneration and necrosis, tubular dilatation, inflammatory cell infiltrates, hyaline cast, and glomerular atrophy were detected in the CP group. It was seen that the CP+Tax group significantly reduced histopathological changes (p<0.001). In addition, immunohistochemically, the expressions of inducible nitric oxide synthase (iNOS) and p53 were highly irregular in the CP group relative to the control groups (p<0.001). Taxifolin treatment (CP+Tax group) significantly decreased the expressions of iNOS and p53 (p<0.001). Current findings revealed nephroprotective and ameliorative effects of Tax against CP-induced kidney toxicity.
Keywords : histopatoloji, iNOS, taksifolin, p53, sisplatin