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通过金属结合,姜黄素可保护大鼠脑匀浆免受铅和镉诱导的脂质过氧化,并保护大鼠脑免受铅诱导的组织损伤。

Through metal binding, curcumin protects against lead- and cadmium-induced lipid peroxidation in rat brain homogenates and against lead-induced tissue damage in rat brain.

作者信息

Daniel Sheril, Limson Janice L, Dairam Amichand, Watkins Gareth M, Daya Santy

机构信息

Department of Biochemistry, Microbiology and Biotechnology and Faculty of Pharmacy, Rhodes University, P.O. Box 94, Grahamstown, South Africa.

出版信息

J Inorg Biochem. 2004 Feb;98(2):266-75. doi: 10.1016/j.jinorgbio.2003.10.014.

DOI:10.1016/j.jinorgbio.2003.10.014
PMID:14729307
Abstract

Curcumin, the major constituent of turmeric is a known, naturally occurring antioxidant. The present study examined the ability of this compound to protect against lead-induced damage to hippocampal cells of male Wistar rats, as well as lipid peroxidation induced by lead and cadmium in rat brain homogenate. The thiobarbituric assay (TBA) was used to measure the extent of lipid peroxidation induced by lead and cadmium in rat brain homogenate. The results show that curcumin significantly protects against lipid peroxidation induced by both these toxic metals. Coronal brain sections of rats injected intraperitoneally with lead acetate (20 mg/kg) in the presence and absence of curcumin (30 mg/kg) were compared microscopically to determine the extent of lead-induced damage to the cells in the hippocampal CA1 and CA3 regions, and to establish the capacity of curcumin to prevent such damage. Lead-induced damage to the neurons was significantly curtailed in the rats injected with curcumin. Possible chelation of lead and cadmium by curcumin as its mechanism of neuroprotection against such heavy metal insult to the brain was investigated using electrochemical, ultraviolet spectrophotometric and infrared spectroscopic analyses. The results of the study show that there is an interaction between curcumin and both cadmium and lead, with the possible formation of a complex between the metal and this ligand. These results imply that curcumin could be used therapeutically to chelate these toxic metals, thus potentially reducing their neurotoxicity and tissue damage.

摘要

姜黄素是姜黄的主要成分,是一种已知的天然抗氧化剂。本研究考察了该化合物对雄性Wistar大鼠海马细胞铅诱导损伤的保护能力,以及对大鼠脑匀浆中铅和镉诱导的脂质过氧化的保护能力。采用硫代巴比妥酸测定法(TBA)来测量大鼠脑匀浆中铅和镉诱导的脂质过氧化程度。结果表明,姜黄素能显著保护细胞免受这两种有毒金属诱导的脂质过氧化。对腹腔注射醋酸铅(20 mg/kg)且分别添加和不添加姜黄素(30 mg/kg)的大鼠的冠状脑切片进行显微镜检查,以确定铅对海马CA1和CA3区细胞的损伤程度,并确定姜黄素预防此类损伤的能力。在注射了姜黄素的大鼠中,铅诱导的神经元损伤明显减少。利用电化学、紫外分光光度法和红外光谱分析法研究了姜黄素对铅和镉的可能螯合作用,以此作为其对大脑这种重金属损伤的神经保护机制。研究结果表明,姜黄素与镉和铅之间存在相互作用,金属与该配体可能形成复合物。这些结果表明,姜黄素可用于治疗螯合这些有毒金属,从而有可能降低它们的神经毒性和组织损伤。

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