综述 Review

NADPH氧化酶与脑缺血/再灌注损伤

Published at: 2013年第33卷第3期

张朝弘 1 , 刘丹彦 1
1 重庆医科大学附属第一医院麻醉科,重庆 400016
通讯作者 丹彦 刘 Email: liudanyan418@qq.com
DOI: 10.3978/j.issn.2095-6959.10.3978/j.issn.2095-6959.2013.03.013
基金:

摘要

氧化应激是发生脑缺血/再灌注(ischemia/reperfusion, I/R)损伤的重要机制。近来研究发现,还原型烟酰胺腺嘌呤二核苷酸磷酸(nicotinamide adenine dinucleotide phosphate,NADPH)氧化酶产生的活性氧对脑I/R后的氧化应激起到重要的作用。一些方法(如常压高氧、缺血后处理)和一些药物(如罗布麻宁、替米沙坦、桦木酸、加兰他敏、雷公藤红素等)可以NADPH氧化酶为靶点治疗脑I/R损伤。


NADPH oxidase and cerebral ischemia/reperfusion injury

Abstract

Oxidative stress is an important mechanism for cerebral ischemia/reperfusion(I/R) injury. Recently, studies indicate that reactive oxygen species (ROS) from nicotinamide adenine dinucleotide phosphate (NADPH) oxidase play a very important role in oxidative stress following cerebral ischemia/reperfusion. There are some strategies (such as normobaric hyperoxia, ischemic postconditioning) and some medicines (such as apocynin, telmisartan, betulinic acid, galantamine, celastrol) can reduce cerebral ischemia/reperfusion injury through targeting NADPH oxidase.


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引用

引用本文: 朝弘 张, 丹彦 刘. NADPH氧化酶与脑缺血/再灌注损伤 [J]. 临床与病理杂志, 2013, 33(3): 246-250.
Cite this article as: ZHANG Zhaohong, LIU Danyan . NADPH oxidase and cerebral ischemia/reperfusion injury [J]. Journal of Clinical and Pathological Research, 2013, 33(3): 246-250.