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作 者:赵雅宁[1] 张文丽[1] 田艳霞[1] 崔建忠[2] 高俊玲[1]
机构地区:[1]华北煤炭医学院,河北唐山063000 [2]唐山市工人医院
出 处:《山东医药》2009年第2期15-17,共3页Shandong Medical Journal
基 金:中国人事部留学归国基金资助项目(2007-17);河北省博士基金资助项目(06547008D-7)
摘 要:目的研究弥漫性脑创伤(DBI)后依达拉奉(Edaravone)对大鼠脑组织超微结构及神经功能的影响。方法将雄性SD大鼠随机分为假手术组、创伤组、Edaravone治疗组。Marmarou′s法建立大鼠DBI损伤模型。术后24、48、72 h取大脑海马组织做电镜观察;术后24、48、72 h对大鼠学习记忆功能(水迷宫法)和综合运动功能(转棒法)进行评定。结果电镜下Edaravone治疗组中神经元细胞核、线粒体受损程度均低于创伤组;水迷宫实验显示创伤组大鼠搜索安全岛潜伏期(230.9±20.9)s,假手术组为(50.7±4.9)s,Edaravone治疗组为(70.6±8.7)s,三组比较,P均<0.05;创伤组综合运动能力评分为(79.1±24.5)s,假手术组为(278.6±32.7)s,Edaravone治疗组为(130.0±30.8)s,三组比较,P均<0.05。结论Edaravone可改善DBI后学习记忆功能和综合运动功能,减轻海马神经元超微结构损害程度。Objective To study the effects of Edaravone on neurological function and ultrastructure of brain tissue in rats after diffuse brain injury(DBI). Methods Male Sprague-Dawley rats were randomly divided into three groups:sham operated group,traumatic group, Edaravone treatment group. DBI rat model was established aecoding to the description of Marmarou' s brain injury. The histopathologic changes of hippocampus tissue were observed by electron microscope At 24, 48,72 h after injury. Learning and memory function( Morris water maze) and behavioral tests( rod apparatus method)were performed daily at 24, 48 and 72 h time points. Results At electron microscope level, the damage of nuclear and mitochondria of neurons in Edaravone treatment group was obviously milder than that in traumatic group. The searching safety island period of rats in the traumatic group (230.9 ±20.9) were significantly longer than those of rats in the sham group ( 50.7 ± 4.9 ), while those in the Edaravone group ( 70.6 ± 8.7 ) were shorter than in the traumatic group; The neuroscores of comprehensive movement ability in traumatic group (79.1 ± 24.5 ) was lower those in sham operation group (278.6 ± 32.7 ), while those in Edaravone treatment group ( 130.0 ± 30.8) were restored markedly( P 〈 0.05 ). Conclusion Edaravone can dramatically improve neurological function after DBI and the molecular mechanisms is related to attenuates traumatic cerebral ultrastructure damage following tramatic brain.
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