尿酸在脑缺血再灌注中的神经保护作用  

Neuroprotective effect of uric acid in cerebral ischemia-reperfusion injury

作　　者：沈玲玲 逯丹 李克深[1] 徐安定[1,2] Shen Lingling;Lu Dan;Li Keshen;Xu Anding(Department of Neurology and Stroke Center,the First Affiliated Hospital of Jinan University,Guangzhou 510630,China;Clinical Neuroscience Institute of Jinan University,Guangzhou,510630,China)

机构地区：[1]暨南大学附属第一医院神经内科与脑血管病中心,广州510630 [2]暨南大学临床神经科学研究所,广州510630

出　　处：《国际脑血管病杂志》2018年第9期701-707,共7页International Journal of Cerebrovascular Diseases

基　　金：国家自然科学基金（81671167）;广东省科技计划项目（2017A020215049）;广州市科技计划项目（155700029,1561000289）

摘　　要：尿酸是嘌呤代谢终产物.大量临床研究显示,高水平血清尿酸是急性缺血性卒中患者转归良好的预测指标.氧化应激是脑缺血再灌注损伤的主要机制.作为一种强效抗氧化剂,在血管再通治疗中应用尿酸被认为具有潜在的神经保护作用,但其具体机制尚不清楚.文章就尿酸在脑缺血再灌注损伤中的神经保护作用机制进行了综述,旨在为今后研究和临床实践提供思路.Uric acid is an end product of purine metabolism. A large number of clinical studies have shown that high-level serum uric acid is a good predictor of outcome in patients with acute ischemic stroke. Oxidative stress is the main mechanism of cerebral ischemia-reperfusion injury. As a potent antioxidant, uric acid is considered to have a potential neuroprotective effect in the vascular recanalization treatment, but its specific mechanism remains unclear. This article reviews the neuroprotective mechanism of uric acid in cerebral ischemia-reperfusion injury in order to provide ideas for future research and clinical practice.

关 键 词：脑缺血 再灌注损伤 卒中 尿酸 氧化应激 抗氧化剂 神经保护药 

分 类 号：R743[医药卫生—神经病学与精神病学]