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Role of nitric oxide synthesis inhibitors in iron-induced nigral neurotoxicity: a mechanistic exploration.一氧化氮合酶抑制剂在铁诱导的黑质神经毒性中的作用:一种机制探讨。
Toxicol Mech Methods. 2008;18(4):379-84. doi: 10.1080/15376510801891369.
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Nitric oxide synthesis inhibition attenuates iron-induced neurotoxicity: a stereological study.一氧化氮合成抑制减轻铁诱导的神经毒性:一项体视学研究。
Neurotoxicology. 2008 Jan;29(1):130-5. doi: 10.1016/j.neuro.2007.10.003. Epub 2007 Oct 13.
3
Alpha-tocopherol-mediated long-lasting protection against oxidative damage involves an attenuation of calcium entry through TRP-like channels in cultured hippocampal neurons.
Free Radic Biol Med. 2007 May 1;42(9):1326-37. doi: 10.1016/j.freeradbiomed.2007.01.032. Epub 2007 Jan 23.
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Vitamin E intake and quality of life in amyotrophic lateral sclerosis patients: a follow-up case series study.肌萎缩侧索硬化症患者的维生素E摄入量与生活质量:一项随访病例系列研究。
Neurol Sci. 2006 Jul;27(3):190-3. doi: 10.1007/s10072-006-0668-x.
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A calcium channel blocker flunarizine attenuates the neurotoxic effects of iron.一种钙通道阻滞剂氟桂利嗪可减轻铁的神经毒性作用。
Cell Biol Toxicol. 2006 Mar;22(2):119-25. doi: 10.1007/s10565-006-0037-9. Epub 2006 Mar 9.
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Vitamin E supplementation in Alzheimer's disease, Parkinson's disease, tardive dyskinesia, and cataract: Part 2.维生素E补充剂在阿尔茨海默病、帕金森病、迟发性运动障碍和白内障中的应用:第2部分。
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A transient treatment of hippocampal neurons with alpha-tocopherol induces a long-lasting protection against oxidative damage via a genomic action.用α-生育酚对海马神经元进行短暂处理,可通过基因组作用诱导对氧化损伤的长期保护。
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Vitamin E and donepezil for the treatment of mild cognitive impairment.维生素E与多奈哌齐治疗轻度认知障碍
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High dose vitamin E therapy in amyotrophic lateral sclerosis as add-on therapy to riluzole: results of a placebo-controlled double-blind study.高剂量维生素E疗法作为利鲁唑的附加疗法用于肌萎缩侧索硬化症:一项安慰剂对照双盲研究的结果
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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.

DOI:10.1007/s10571-009-9461-8
PMID:19798567
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11498760/
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。