Astilbin ameliorates cisplatin-induced nephrotoxicity through reducing oxidative stress and inflammation.
Food Chem Toxicol
; 114: 227-236, 2018 Apr.
Article
em En
| MEDLINE
| ID: mdl-29471006
ABSTRACT
Oxidative stress and inflammation are considered to be the main pathogenesis of cisplatin nephrotoxicity. Astilbin, a flavonoid with anti-oxidation and anti-inflammation function, has been used to treat heavy metal induced kidney injury. In this study, we investigated the protective effects of astilbin on cisplatin-induced nephrotoxicity and its underlying mechanisms. Our results showed that astilbin markedly inhibited cisplatin-induced cell apoptosis and recovered cell growth. Astilbin significantly decreased reactive oxygen species (ROS) accumulation and alleviated ROS-induced activation of p53, MAPKs and AKT signaling cascades, which in turn attenuated cisplatin-induced HEK-293â¯cell apoptosis. Astilbin effectively enhanced NRF2 activation and transcription of its targeting antioxidant genes to reduce ROS accumulation in cisplatin-induced HEK-293â¯cells. Furthermore, we found that astilbin obviously suppressed tumor necrosis factor alpha (TNF-α) expression and NF-κB activation, and also inhibited the expression of induced nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Finally, we confirmed that the effect of astilbin to improve renal oxidative stress and inflammation in cisplatin induced acute nephrotoxic mice. In conclusion, our study suggests that astilbin could ameliorate the cisplatin-induced nephrotoxicity by reducing oxidative stress and inflammation.
Palavras-chave
Texto completo:
1
Bases de dados:
MEDLINE
Assunto principal:
Cisplatino
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Estresse Oxidativo
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Flavonóis
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Nefropatias
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Antineoplásicos
Limite:
Animals
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Humans
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Male
Idioma:
En
Revista:
Food Chem Toxicol
Ano de publicação:
2018
Tipo de documento:
Article
País de afiliação:
China