氨基胍对大鼠脑缺血线粒体损伤的作用  

Effect of Aminoguanidine on Mitochondria Injury in Cerebral Ischemia Rats

作　　者：侯量[1] 尚涛[2] 尹来波[1] 朱佳龙[1] 吴勇娟[1] 

机构地区：[1]石河子大学医学院第一附属医院心胸外科,新疆石河子832008 [2]河北医科大学附属石家庄市第三医院,河北石家庄050011

出　　处：《医学信息》2012年第9期114-115,共2页Journal of Medical Information

摘　　要：目的观察氨基胍（AG）对大鼠局灶性脑缺血线粒体损伤的作用。方法将大鼠随机分为假手术组、缺血对照组、AG治疗组，采用线栓法复制大鼠大脑中动脉栓塞（MCAO）模型，分别于缺血后2、6、12h给药治疗3d，提取缺血侧脑组织线粒体，测定线粒体总ATP酶、超氧化物歧化酶（SOD）7％一氧化氮（NO）、丙二醛（MDA）含量。结果在大鼠MCAO后线粒体No生成明显增加，线粒体总ATP酶、soD活性均明显下降，线粒体MDA含量明显升高：缺血2、6、12h给予AG治疗3d与缺血对照组相比NO生成有所下降，总ATP酶、SOD活性均升高，MDA含量下降。结论AG能明显抑制大鼠脑缺血后线粒体No生成，增加线粒体能量供应及抗氧化作用，减轻脑缺血损伤。Objective To examine the effect of aminoguanidine（AG） on mitochondria injury in focal cerebral ischemia rats.Methods Rats were randomly devided into sham, ischemia and AG treatment groups. The model of focal cerebral ischemia in rats was prepared with thread embolism. AG was administered respectively at 2, 6, 12h after MCAO. Rats were killed and mitochondria of cerebral tissue were isolated with differential centrifugation 3d after AG treatment.Activities of ATPase, SOD and contents of NO and MDA in mitochondria were measured. Results The contents of mitochondria NO and MDA markedly increased,the activities of mitochondria ATPase and SOD markedly decreased in MCAO rats. Compared with ischemia group, the activities of ATPase and SOD in mitochondfia enhanced and the contents of NO and MDA in mitochondria decreased in ischemia 2, 6, 12h group administered with AG. Conclusion AG can inhibit the production of NO,beneficially improve mitochondria energy pump and ameliorate oxidative, and effectively protect brain damage induced by cerebral ischemia.

关 键 词：氨基胍 脑缺血 线粒体 一氧化氮 

分 类 号：R944.27[医药卫生—药剂学]