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癫痫实验模型中与神经元凋亡相关的氧化应激。

Oxidative stress associated with neuronal apoptosis in experimental models of epilepsy.

机构信息

Laboratorio de Neuropatología Experimental, Instituto Nacional de Neurología y Neurocirugía, Manuel Velasco Suárez, Insurgentes Sur 3877, La Fama, CP 14269, Tlalpan, DF, Mexico.

Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México (UNAM), Avenida Universidad 3000, CP 04510, Coyoacán, DF, Mexico.

出版信息

Oxid Med Cell Longev. 2014;2014:293689. doi: 10.1155/2014/293689. Epub 2014 Dec 29.

DOI:10.1155/2014/293689
PMID:25614776
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4295154/
Abstract

Epilepsy is considered one of the most common neurological disorders worldwide. Oxidative stress produced by free radicals may play a role in the initiation and progression of epilepsy; the changes in the mitochondrial and the oxidative stress state can lead mechanism associated with neuronal death pathway. Bioenergetics state failure and impaired mitochondrial function include excessive free radical production with impaired synthesis of antioxidants. This review summarizes evidence that suggest what is the role of oxidative stress on induction of apoptosis in experimental models of epilepsy.

摘要

癫痫被认为是全球最常见的神经障碍之一。自由基产生的氧化应激可能在癫痫的发生和发展中起作用；线粒体和氧化应激状态的改变可导致与神经元死亡途径相关的机制。生物能量状态衰竭和线粒体功能受损包括自由基产生过多，抗氧化剂合成受损。这篇综述总结了证据，表明氧化应激在癫痫实验模型中诱导细胞凋亡的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffd8/4295154/6fca631e012e/OMCL2014-293689.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffd8/4295154/8563f1b18145/OMCL2014-293689.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffd8/4295154/6fca631e012e/OMCL2014-293689.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffd8/4295154/8563f1b18145/OMCL2014-293689.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffd8/4295154/6fca631e012e/OMCL2014-293689.002.jpg

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