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颞叶癫痫患者金属硫蛋白的免疫组织化学研究

Immunohistochemical study of Metallothionein in patients with temporal lobe epilepsy.

作者信息

Juárez-Rebollar Daniel, Alonso-Vanegas Mario, Nava-Ruíz Concepción, Buentello-García Masao, Yescas-Gómez Petra, Díaz-Ruíz Araceli, Rios Camilo, Méndez-Armenta Marisela

机构信息

Lab. Neuropatología Experimental, Instituto Nacional de Neurología y Neurocirugía MVS, Mexico.

Subdirección de Neurocirugía, Instituto Nacional de Neurología y Neurocirugía MVS, Mexico.

出版信息

J Clin Neurosci. 2017 May;39:87-90. doi: 10.1016/j.jocn.2016.12.016. Epub 2017 Jan 10.

DOI:10.1016/j.jocn.2016.12.016
PMID:28087193
Abstract

Epilepsy is characterized by spontaneous recurrent seizures and temporal lobe epilepsy (TLE) is the most common serious neurological example of acquired and frequent epilepsy. Oxidative stress is recognized as playing a contributing role in several neurological disorders, and most recently have been implicated in acquired epilepsies. The MTs occur in several brain regions and may serve as neuroprotective proteins against reactive oxygen species causing oxidative damage and stress. The main aim of this work was to describe the immunohistochemical localization of MT in the specimens derived from the patients affected by TLE. Histopathological examination showed NeuN, GFAP and MT immunopositive cells that were analyzed for determinate in hippocampal and parietal cortex samples. An increase in the reactive gliosis associated with increased MT expression was observed in patients with TLE.

摘要

癫痫的特征是自发性反复发作,而颞叶癫痫(TLE)是获得性频繁癫痫最常见的严重神经学实例。氧化应激被认为在几种神经疾病中起作用,最近还与获得性癫痫有关。金属硫蛋白(MT)存在于几个脑区,可能作为神经保护蛋白抵御引起氧化损伤和应激的活性氧。这项工作的主要目的是描述MT在TLE患者标本中的免疫组织化学定位。组织病理学检查显示在海马和顶叶皮质样本中对NeuN、GFAP和MT免疫阳性细胞进行分析以确定情况。在TLE患者中观察到与MT表达增加相关的反应性胶质增生增加。

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引用本文的文献

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Neuroglia Cells Transcriptomic in Brain Development, Aging and Neurodegenerative Diseases.脑发育、衰老及神经退行性疾病中的神经胶质细胞转录组学
Aging Dis. 2023 Feb 1;14(1):63-83. doi: 10.14336/AD.2022.0621.
2
Metallothionein in Brain Disorders.金属硫蛋白在脑部疾病中的作用
Oxid Med Cell Longev. 2017;2017:5828056. doi: 10.1155/2017/5828056. Epub 2017 Sep 20.