6-羟基褪黑素保护神经细胞抗缺血再灌注损伤的作用机制  

The role of 6-hydroxylmelatonin protecting neurons from ischemia-reperfusion-mediated injurys

作　　者：段秋红[1] 王剑飞[1] 卢涛[1] 王西明[1] 

机构地区：[1]华中科技大学同济医学院生物化学与分子生物学系,武汉430030

出　　处：《卒中与神经疾病》2008年第1期45-48,共4页Stroke and Nervous Diseases

摘　　要：目的探讨6-羟基褪黑素的神经保护作用及作用机理。方法体外培养神经母细胞瘤N2a细胞,缺糖、缺血清和缺氧(OGSD)90min,再正常培养不同时间,同时加入6-羟基褪黑素,观察细胞生存能力(MTT法)、线粒体跨膜电位变化(荧光标记)、线粒体细胞色素C释放(western blot)、caspase 3活性(荧光底物)以及细胞内活性氧(荧光标记)的产生。结果6-羟基褪黑素抑制细胞色素C释放,抑制caspase 3激活,清除细胞内活性氧,稳定线粒体跨膜电位。结论6-羟基褪黑素通过直接抗氧化作用和抑制线粒体凋亡途径促进神经细胞生存。Objective The protective role of 6-hydroxylmelatonin（6-HOMel） was determined in N2a cells following exposure to oxygen-glucose-serum deprivation （OGSD）-reperfusion insults. Methods After cultured N2a in vitro was deprived of glucose, serum and oxygen for 90 min, the different concentrations 6-HOMel were added to normal medium. Then, treated cells were normally cultured for different time. At the end of the treatment, the cultural solution was collected in analysis of lactate dehydrogenase（LDH） activity and the cells were processed to examine the following indications; cell viability（MTT）, ROS production, mitochondrial transmembrane potential（△ψm）,cytochrome c（cyt c） and caspase3 activity. Results 6-HOMel promoted N2a cell survival following OGSD-reperfusion-mediated damage by directly scavenging ROS and inhibiting cyt c release from mitochondria and caspase3 activity. Conclusions The results of the present investigation emphasize the potential use of 6-HOMel as a supplement in the therapy of neurological disorders in which oxidative stress is involved.

关 键 词：6-羟基褪黑素 神经细胞细胞色素C 缺血再灌注 细胞凋亡 

分 类 号：R743[医药卫生—神经病学与精神病学]