检索规则说明:AND代表“并且”;OR代表“或者”;NOT代表“不包含”;(注意必须大写,运算符两边需空一格)
检 索 范 例 :范例一: (K=图书馆学 OR K=情报学) AND A=范并思 范例二:J=计算机应用与软件 AND (U=C++ OR U=Basic) NOT M=Visual
机构地区:[1]中国医科大学附属第一医院神经内科,辽宁沈阳110001 [2]中国医科大学附属第一医院神经生物学教研室,辽宁沈阳110001
出 处:《中国应用生理学杂志》2010年第2期144-146,257,共3页Chinese Journal of Applied Physiology
基 金:国家自然基金资助项目(30700938,30872656,30700861);辽宁省自然基金资助(20082078,20062102)
摘 要:目的:观察脑缺血/再灌注(CI/R)早期缺血区脑组织的内皮型一氧化氮合酶(eNOS)与神经型一氧化氮合酶(nNOS)表达的变化。方法:健康wistar大鼠60只,体重200~280g,由中国医科大学动物中心提供,雌雄各半。随机分为6组(n=10):假手术组、缺血1h组、缺血2h组、再灌注0.5h组、再灌注1h组、再灌注2h组。采用线栓法制作大鼠CI/R模型,免疫组化方法检测缺血区脑组织的eNOS与nNOS蛋白表达情况。结果:与假手术组比较,CI/R模型大鼠脑组织血管内皮细胞内eNOS表达在缺血1h内升高,之后到再灌注2h内持续降低。而nNOS的表达在缺血到再灌注2h内持续上升。结论:CI/R模型中缺血区脑组织的eNOS与nNOS的变化趋势不同,表明一氧化氮在缺血性脑损伤病理过程的作用与一氧化氮合酶亚型的变化有关。Objective:To observe the expression of endothelial nitric oxide synthase (eNOS)and nervous nitric oxide synthase (nNOS) in rats during cerebral ischemia/reperfusion (CI/R) and study if change will be happen in subgroup between eNOS and nNOS during earlier period of CI/R.Methods:A total of 60 Wistar rats weighting 200~280 g,supplied by Animal Center of China Medical University,were divided into 6 groups (n=10)(sham operation group;ischemia 1 h、2 h group;reperfusion 0.5 h、1 h、2 h group).Female and male was half-and-half.Cerebral ischemia/reperfusion injury was induced by a 2-hour suture occlusion of the unilateral middle cerebral artery,immediately after suture withdrawal to allow reperfusion,eNOS and nNOS expressions were examined by the method of immunohistochemistry.Results:eNOS expressions increased in 1-hour during ischemia,keeping up with decreasing until reperfusion 2-hour.While nNOS expressions increased in 2-hour between ischemia and reperfusion.Conclusion:Changes of expression between eNOS and nNOS in rats during cerebral ischemia/reperfusion are different.This may be related with ischemia and reperfusion injury.
关 键 词:脑缺血/再灌注 内皮型一氧化氮合酶 神经型一氧化氮合酶 免疫组化
分 类 号:R742[医药卫生—神经病学与精神病学]
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在链接到云南高校图书馆文献保障联盟下载...
云南高校图书馆联盟文献共享服务平台 版权所有©
您的IP:216.73.216.222