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姜黄素减轻庆大霉素诱导的大鼠肾脏氧化损伤。

Curcumin attenuates gentamicin-induced renal oxidative damage in rats.

作者信息

Farombi E O, Ekor M

机构信息

Drug Metabolism and Toxicology Research Laboratories, Department of Biochemistry, College of Medicine, University of Ibadan, Nigeria.

出版信息

Food Chem Toxicol. 2006 Sep;44(9):1443-8. doi: 10.1016/j.fct.2006.05.005. Epub 2006 May 20.

Abstract

The present investigation reports the effect of curcumin, an antioxidant, on gentamicin-induced-renal oxidative damage in rats. Curcumin (200 mg/kg p.o.) was administered for 2 weeks before and 1 week simultaneously with gentamicin (100 mg/kg i.p.). Saline treated rats served as control. Serum creatinine, blood urea (BUN), urinary protein, glucose, urine gamma glutamyl transferase and urine volume increased in rats treated with gentamicin while creatinine clearance decreased compared to controls P<0.001. Renal histological examination revealed tubular necrosis. Curcumin significantly normalized the above parameters. Gentamicin decreased the activities of catalase (CAT), gutathione peroxidase (GSHPx) and the level of glutathione (GSH) but the activity of copper, zinc-superoxide dismutase (Cu, Zn-SOD) was unaltered compared to control. Curcumin attenuated the gentamicin-induced reduction in the activities of CAT, GSHPx and level of GSH by 31%, 55% and 74%, respectively. Curcumin attenuated the gentamicin-induced increases in both plasma malondialdehyde (MDA) and kidney MDA by 57% and 62%, respectively, as well as lipid hydroperoxide (LOOH) formation by 52% and 56% in rat plasma and kidney, respectively. However, Curcumin did not reduce gentamicin-induced formation of LOOH, both in the plasma and kidney, in the presence of exogenous oxidants (1 mM FeSO4, 1 mM ascorbate, 0.2 mM H2O2). Our data indicate that the natural antioxidant curcumin can be a potent protective agent against renal oxidative damage mediated by gentamicin.

摘要

本研究报告了抗氧化剂姜黄素对庆大霉素诱导的大鼠肾氧化损伤的影响。在给予庆大霉素(100 mg/kg腹腔注射)前2周及同时给予1周期间,口服给予姜黄素(200 mg/kg)。用生理盐水处理的大鼠作为对照。与对照组相比,庆大霉素处理的大鼠血清肌酐、血尿素(BUN)、尿蛋白、葡萄糖、尿γ-谷氨酰转移酶和尿量增加,而肌酐清除率降低(P<0.001)。肾脏组织学检查显示肾小管坏死。姜黄素使上述参数显著恢复正常。庆大霉素降低了过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSHPx)的活性以及谷胱甘肽(GSH)的水平,但与对照组相比,铜锌超氧化物歧化酶(Cu, Zn-SOD)的活性未改变。姜黄素分别使庆大霉素诱导的CAT、GSHPx活性降低以及GSH水平降低减弱了31%、55%和74%。姜黄素分别使庆大霉素诱导的血浆丙二醛(MDA)和肾脏MDA增加减弱了57%和62%,以及大鼠血浆和肾脏中脂质氢过氧化物(LOOH)的形成分别减弱了52%和56%。然而,在存在外源性氧化剂(1 mM硫酸亚铁、1 mM抗坏血酸、0.2 mM过氧化氢)的情况下,姜黄素并未降低庆大霉素诱导的血浆和肾脏中LOOH的形成。我们的数据表明,天然抗氧化剂姜黄素可能是对抗庆大霉素介导的肾氧化损伤的有效保护剂。

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