银杏
肌酐
丙二醛
肾毒性
血尿素氮
肾
肾功能
毒性
谷胱甘肽
药理学
化学
内科学
肝功能
内分泌学
氧化应激
医学
生物化学
酶
作者
Kürşad Yapar,Kültiğin Çavuşoğlu,Ertan Oruç,Emine Yalçın
出处
期刊:Journal of Medicinal Food
[Mary Ann Liebert]
日期:2010-02-01
卷期号:13 (1): 179-188
被引量:50
标识
DOI:10.1089/jmf.2009.0028
摘要
The aim of the present study was to investigate the protective role of Ginkgo biloba leaf extract against uranium (U)-induced toxicity in Swiss albino mice. The mice were randomly divided into six groups, each consisting of six animals: Group I (control) received tap water alone, Group II received U at a dose of 5 mg/kg of body weight, Group III received G. biloba at a dose of 50 mg/kg of body weight, Group IV received G. biloba at a dose of 150 mg/kg of body weight, Group V received G. biloba (50 mg/kg of body weight) and U (5 mg/kg of body weight), and Group VI received G. biloba (150 mg/kg of body weight) and U (5 mg/kg of body weight) by oral gavage for 5 days. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN), and creatinine levels were determined to assess liver and kidney function, respectively. Also, liver and kidney samples were taken for the determination of tissue malondialdehyde (MDA) and reduced glutathione (GSH) levels, and histopathological changes in liver and kidneys were investigated. The results indicated that there was a significant increase (P < .05) in selected serum parameters. Serum AST, ALT, BUN, and creatinine levels significantly increased in mice treated with U alone when compared to the other groups. Moreover, U-induced oxidative damage caused a significant decrease in GSH levels and a significant increase in MDA levels of liver and kidney tissues. Treatment with G. biloba produced amelioration in biochemical indices of hepatotoxicity and nephrotoxicity according to Group II. Each dose of G. biloba provided significant protection against U-induced toxicity, and its strongest effect was observed at a dose of 150 mg/kg of body weight. In vivo results showed that G. biloba extract is a potent protector against U-induced toxicity, and its protective role is dose-dependent.
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