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

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...

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Veröffentlicht in:Etlik Veteriner Mikrobiyoloji Dergisi 2024-07, Vol.35 (1), p.1-7
Hauptverfasser: Akçakavak, Gökhan, Karataş, Özhan, Çelik, Zeynep, Tural, Ayşenur, Dağar, Osman, Abduljabbar, Ahmed, Kılınç, Bahadır, Tuzcu, Mehmet
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container_title Etlik Veteriner Mikrobiyoloji Dergisi
container_volume 35
creator Akçakavak, Gökhan
Karataş, Özhan
Çelik, Zeynep
Tural, Ayşenur
Dağar, Osman
Abduljabbar, Ahmed
Kılınç, Bahadır
Tuzcu, Mehmet
description 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
doi_str_mv 10.35864/evmd.1458328
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title Taxifolin attenuates cisplatin-induced kidney damage in rats via suppressing p53 and iNOS
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