氧化应激在神经变性中的潜在作用：机制综述。
The Underlying Role of Oxidative Stress in Neurodegeneration: A Mechanistic Review.
机构信息
Neurosciences Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran.
Chronic Kidney Disease Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
出版信息
CNS Neurol Disord Drug Targets. 2018;17(3):207-215. doi: 10.2174/1871527317666180425122557.
BACKGROUND
Neurodegeneration is a condition in which progressive loss of function and structure of neurons occurs. Several lines of evidence suggest that oxidative stress has a central role in neurodegenerative diseases.
OBJECTIVE
The aim was to survey molecular mechanisms underlying the involvement of oxidative stress in developing different neurodegenerative diseases.
METHODS
Original and review articles were retrieved through a PubMed and Google scholar search (from 1989 to 2015) using the following key words: "oxidative stress", "nerve degeneration" and "neurodegenerative diseases".
RESULTS
A comprehensive analysis of the obtained articles confirmed strong involvement of oxidative stress in the pathophysiology of neurodegenerative diseases through a variety of mechanisms including induction of oxidation of nucleic acids, proteins and lipids, formation of advanced glycation end products, mitochondrial dysfunction, glial cell activation, amyloid β deposition and plaque formation, apoptosis, cytokine production and inflammatory responses, and proteasome dysfunction.
CONCLUSION
Regarding the pivotal role of oxidative stress in neurodegeneration, modulation of free radical production or alleviating their harmful effects can be considered as a potential therapeutic strategy for preventing and controlling neurodegenerative diseases. Accordingly; boosting endogenous antioxidant capacity besides providing exogenous sources of antioxidants merits future research in order to discover new therapeutic agents.
背景
神经退行性变是一种神经元功能和结构进行性丧失的疾病。有几条证据表明氧化应激在神经退行性疾病中起核心作用。
目的
旨在调查氧化应激参与不同神经退行性疾病发展的分子机制。
方法
通过 PubMed 和 Google scholar 搜索（1989 年至 2015 年），使用以下关键词检索原始和综述文章：“氧化应激”、“神经变性”和“神经退行性疾病”。
结果
对获得的文章进行综合分析证实，氧化应激通过多种机制（包括核酸、蛋白质和脂质氧化的诱导、晚期糖基化终产物的形成、线粒体功能障碍、胶质细胞激活、β淀粉样蛋白沉积和斑块形成、细胞凋亡、细胞因子产生和炎症反应以及蛋白酶体功能障碍）强烈参与神经退行性疾病的病理生理学。
结论
鉴于氧化应激在神经退行性变中的关键作用，调节自由基的产生或减轻其有害影响可以被认为是预防和控制神经退行性疾病的一种潜在治疗策略。因此，增强内源性抗氧化能力，除了提供外源性抗氧化剂来源外，值得未来进行研究，以发现新的治疗剂。
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