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姜黄素可改善双氯芬酸钠诱导的雄性白化大鼠肾毒性。

Curcumin ameliorates diclofenac sodium-induced nephrotoxicity in male albino rats.

作者信息

Ahmed Ahmady Y, Gad Amany M, El-Raouf Ola M Abd

机构信息

Department of Pharmacology, National Organization for Drug Control and Research, NODCAR, Giza, Egypt.

出版信息

J Biochem Mol Toxicol. 2017 Oct;31(10). doi: 10.1002/jbt.21951. Epub 2017 Aug 11.

DOI:10.1002/jbt.21951
PMID:28800174
Abstract

Exposure to drugs often results in toxicity in the kidney which represents the major control system maintaining homeostasis of the body and thus is especially susceptible to xenobiotics. Nephrotoxicity is a life-threatening side-effect of nonsteroidal anti-inflammatory drugs (NSAIDs). Diclofenac is one of the most frequently prescribed NSAIDs and have been reported to cause multiple organs damage. Curcumin (CUR) exhibits nephroprotective properties. Therefore, rats were divided into four groups; rats of groups 3 and 4 received diclofenac (100 mg/kg, i.m.), whereas rats of groups 2 and 4 received CUR (100 mg/kg, p.o.) for 3 days. Diclofenac revealed a significant increase in urea and creatinine levels and malondialdehyde concentration and marked reduction in catalase activity and reduced glutathione concentration. Histopathologically, diclofenac produced fatty changes and eosinophilic casts were detected in the renal tubules, those were attenuated by administration of CUR prior diclofenac.

摘要

接触药物常常会导致肾脏中毒,肾脏是维持身体内环境稳态的主要控制系统,因此特别容易受到外源性物质的影响。肾毒性是非甾体抗炎药(NSAIDs)危及生命的副作用。双氯芬酸是最常处方的NSAIDs之一,据报道会导致多器官损伤。姜黄素(CUR)具有肾保护特性。因此,将大鼠分为四组;第3组和第4组大鼠接受双氯芬酸(100mg/kg,肌肉注射),而第2组和第4组大鼠接受姜黄素(100mg/kg,口服),持续3天。双氯芬酸使尿素和肌酐水平以及丙二醛浓度显著升高,过氧化氢酶活性和还原型谷胱甘肽浓度显著降低。组织病理学上,双氯芬酸导致脂肪变性,肾小管中检测到嗜酸性管型,在双氯芬酸给药前给予姜黄素可减轻这些变化。

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