naphthoflavoneprotectsmicefromaristolochicacidlinducedacutekidneyinjuryinacyp1adependentmechanism
文献类型：期刊论文
| 作者 | Ying XIAO1; Xiang XUE1; Yuanfeng WU1; GuozhengXIN1; Yong QIAN2; Tianpei XIE2; Likun GONG1 ; Jin REN1
|
| 刊名 | actapharmacologicasinica
 |
| 出版日期 | 2009 |
| 卷号 | 30期号:11页码:1559 |
| 关键词 | aristolochic acid kidney injury beta-naphthoflavone biotransformation CYP1A |
| ISSN号 | 1671-4083 |
| 英文摘要 | Aim: The role of CYP1A in the protection of aristolochic acid (AA)l-induced nephrotoxicity has been suggested. In the present study we investigated the effects of P-naphthoflavone (BNF), a non-carcinogen CYP1A inducer, on Aal-induced kidney injury.Methods: Mice were pretreated with 80 mg/kg BNF by daily intraperitoneal injection (ip) for 3 days followed by a single ip of 10 mg/kg AAI. AAI and its major metabolites in blood, liver and kidney, the expression of CYP1A1 and CYP1A2 in microsomes of liver and kidney, as well as the nephrotoxicity were evaluated.Results: BNF pretreatment prevented Aal-induced renal damage by facilitating the disposal of AAI in liver. BNF pretreatment induced the expression of CYP1A1 in both liver and kidney; but the induction of CYP1A2 was only observed in liver. Conclusion: BNF prevents Aal-induced kidney toxicity primarily through CYP1A induction. |
| 语种 | 英语 |
| 源URL | [http://119.78.100.183/handle/2S10ELR8/285090]  |
| 专题 | 中国科学院上海药物研究所 |
| 作者单位 | 1.中国科学院上海药物研究所 2.Shanghai TenGen Biomedical Co Ltd, China |
| 推荐引用方式 GB/T 7714 | Ying XIAO,Xiang XUE,Yuanfeng WU,et al. naphthoflavoneprotectsmicefromaristolochicacidlinducedacutekidneyinjuryinacyp1adependentmechanism[J]. actapharmacologicasinica,2009,30(11):1559. |
| APA | Ying XIAO.,Xiang XUE.,Yuanfeng WU.,GuozhengXIN.,Yong QIAN.,...&Jin REN.(2009).naphthoflavoneprotectsmicefromaristolochicacidlinducedacutekidneyinjuryinacyp1adependentmechanism.actapharmacologicasinica,30(11),1559. |
| MLA | Ying XIAO,et al."naphthoflavoneprotectsmicefromaristolochicacidlinducedacutekidneyinjuryinacyp1adependentmechanism".actapharmacologicasinica 30.11(2009):1559. |
入库方式： OAI收割
来源：上海药物研究所
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