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α-生育酚可减少铁诱导的海马和黑质神经元丢失。

Alpha-tocopherol decreases iron-induced hippocampal and nigral neuron loss.

机构信息

School of Health, Hitit University, 19100, Corum, Turkey.

出版信息

Cell Mol Neurobiol. 2010 Apr;30(3):389-94. doi: 10.1007/s10571-009-9461-8. Epub 2009 Oct 2.

Abstract

There are many studies about iron-induced neuronal hyperactivity and oxidative stress. Some reports also showed that iron levels rise in the brain in some neurodegenerative diseases such as Parkinson's (PD) and Alzheimer's disease (AD). It has been suggested that excessive iron level increases oxidative stress and causes neuronal death. Tocopherols act as a free radical scavenger when phenoxylic head group encounters a free radical. We have aimed to identify the effect of alpha-tocopherol (Vitamin E) on iron-induced neurotoxicity. For this reason, rats were divided into three groups as control, iron, and iron + alpha-tocopherol groups. Iron chloride (200 mM in 2.5 microl volume) was injected into brain ventricle of iron and iron + alpha-tocopherol group rats. Same volume of saline (2.5 microl) was given to the rats belonging to control group. Rats of iron + alpha-tocopherol group received intraperitoneally (i.p.) alpha-tocopherol (100 mg/kg/day) for 10 days. After 10 days, rats were perfused intracardially under deep urethane anesthesia. Removed brains were processed using standard histological techniques. The numbers of neurons in hippocampus and substantia nigra of all rats were estimated by stereological techniques. Results of present study show that alpha-tocopherol decreased hippocampal and nigral neuron loss from 51.7 to 12.1% and 41.6 to 17.8%, respectively. Findings of the present study suggest that alpha-tocopherol may have neuroprotective effects against iron-induced hippocampal and nigral neurotoxicity and it may have a therapeutic significance for neurodegenerative diseases involved iron.

摘要

有许多关于铁诱导神经元过度活跃和氧化应激的研究。一些报告还表明,在一些神经退行性疾病中,如帕金森病(PD)和阿尔茨海默病(AD),大脑中的铁含量会升高。有人认为,过量的铁水平会增加氧化应激,导致神经元死亡。生育酚在酚氧基头部基团遇到自由基时充当自由基清除剂。我们旨在确定α-生育酚(维生素 E)对铁诱导神经毒性的影响。为此,将大鼠分为对照组、铁组和铁+α-生育酚组三组。将氯化铁(2.5 微升体积 200mM)注入铁和铁+α-生育酚组大鼠的脑室。对照组大鼠给予相同体积的生理盐水(2.5 微升)。铁+α-生育酚组大鼠腹腔内(i.p.)给予α-生育酚(100mg/kg/天)10 天。10 天后,大鼠在深度氨基甲酸乙酯麻醉下心脏灌流。取出大脑,用标准组织学技术处理。通过立体学技术估计所有大鼠海马和黑质神经元的数量。本研究的结果表明,α-生育酚使海马和黑质神经元的丢失从 51.7%减少到 12.1%和 41.6%减少到 17.8%。本研究的结果表明,α-生育酚可能对铁诱导的海马和黑质神经毒性具有神经保护作用,并且可能对涉及铁的神经退行性疾病具有治疗意义。

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