NNMS抑制大鼠脑缺血再灌注后氧自由基产生的作用  

NNMS reduce the production of ROS after rat cerebral ischemia-reperfusion

作　　者：沈明[1] 徐建兴[2] 

机构地区：[1]北京大学人民医院神经内科,北京100044 [2]中国科学院生物物理所,北京100044

出　　处：《神经科学通报》2005年第1期44-47,共4页Neuroscience Bulletin

摘　　要：目的观察NNMS(3硝基N甲基水杨酰胺)在大鼠脑缺血再灌注过程中减少线粒体氧自由基产生的作用。方法采用线栓法制备大鼠脑缺血再灌注模型,用化学发光法检测体外线粒体产生超氧阴离子和过氧化氢。在2h脑缺血再灌注前静脉注射NNMS,观察在再灌注不同时期缺血脑组织线粒体产生超氧阴离子和过氧化氢的情况。结果在2h局灶脑缺血后再灌注5～40min,缺血区脑组织线粒体产生的超氧阴离子和过氧化氢显著增加,在相应的NNMS给药组,线粒体产生的超氧阴离子和过氧化氢较假处理组均无显著变化。结论再灌注前静脉注射NNMS可以减少再灌注过程中线粒体产生的超氧阴离子和过氧化氢。Objective To study the inhibitory effect of NNMS on the production of reactive oxygen species in mitochondria during cerebral ischemia and reperfusion. Methods Rats middle cerebral artery ischemia-reperfusion model was induced by intraluminal method. The superoxide anions and hydrogen peroxide produced by mitochondria were monitored with the use of chemiluminescence methods. Before reperfusion, animals were treated with NNMS, the O -· 2, H 2O 2 production level of brain tissue from ischemic area were monitored. Results During 5-40min reperfusion after 2 hours ischemia, mitochondria from ischemic areas produce significantly more O -· 2 and H 2O 2but in NNMS administered groups, it was not different compared with control groups. Conclusion NNMS has the potency to inhibit the production of superoxide anion and hydrogen peroxide in mitochondria during the ischemia and reperfusion.

关 键 词：脑缺血 再灌注损伤 氧自由基 线粒体 

分 类 号：R743[医药卫生—神经病学与精神病学]