线粒体自噬在褪黑素抗缺血再灌注损伤中的作用  

Mitophagy play a role in protecting neurons against ischemia/reperfusion-mediated injury directed by melatonin

作　　者：王忠强[1] 段秋红[2] 王剑飞[2] 唐忠志[1] 陈谦[1] 王西明[2] 

机构地区：[1]中国人民解放军广州军区武汉总医院急诊科,武汉430070 [2]华中科技大学同济医学院生物化学与分子生物学系

出　　处：《卒中与神经疾病》2007年第5期296-298,共3页Stroke and Nervous Diseases

摘　　要：目的初步探讨线粒体自体吞噬在褪黑素抗缺血再灌注损伤中的作用。方法体外培养N2a细胞,模拟缺血再灌注,加入褪黑素(melatonin,Mel),用DNA琼脂糖凝胶电泳和Caspase3活性测定分析细胞凋亡情况,并采用激光共聚焦分析线粒体自噬现象。结果(1)Mel能抑制缺血再灌注介导的N2a细胞caspase3的活性,并减轻N2a细胞DNA的片段化;(2)N2a细胞缺血90min再灌注12h,未观察到线粒体自噬现象,而加入Mel的N2a有大量的线粒体自噬现象。结论线粒体自噬可能是褪黑素抗缺血再灌注损伤的机制之一。Objective To explore the protective effect of exogenous melatonin （Mel） on neurons were examined in N2a cells following exposure to oxygen-glucose-serum deprivation （OGSD） insults. Methods After N2a cells cultured in vitro were deprived of glucose, serum and oxygen for 90 min, Mel were added to medium. Then, treated cells were cultured for different intervals. At the end of the treatment, the collected culture solution was used the examination of the following parameters： DNA fragmentation, caspase 3 activity and laser confocal scanning. Results The results show that Mel reduced OGSD mediated N2a cell apoptosis,accordingly the phenomenon of mitophagy was examinated. Conclusions Our study showed that mitophagy maybe play a role in protecting neurons against ischemia/reperfusion injury,although awaiting further study.

关 键 词：褪黑素 神经元 缺血再灌注 线粒体自噬 

分 类 号：R743[医药卫生—神经病学与精神病学]