NADPH氧化酶与脑缺血/再灌注损伤
| 作者: |
1张朝弘,
1刘丹彦
1 重庆医科大学附属第一医院麻醉科，重庆 400016 |
| 通讯: |
刘丹彦
Email: liudanyan418@qq.com |
| DOI: | 10.3978/j.issn.2095-6959.2013.03.013 |
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。
关键词：
NADPH氧化酶；活性氧；脑缺血/再灌注损伤
NADPH oxidase and cerebral ischemia/reperfusion injury
CorrespondingAuthor: LIU Danyan Email: liudanyan418@qq.com
DOI: 10.3978/j.issn.2095-6959.2013.03.013
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.