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作 者:王爱萍[1] 贺湘英[1] 莫亚雄[1] 梁琨[1]
机构地区:[1]昆明医学院第一附属医院,云南昆明650032
出 处:《昆明医学院学报》2010年第1期15-18,共4页Journal of Kunming Medical College
基 金:云南省自然科学基金资助项目(2004C0019R)
摘 要:目的通过脑内注射神经兴奋毒素鹅膏蕈氨酸(ibotenateacid,IA)建立新生小鼠脑白质损伤模型,为新生儿兴奋毒性脑白质损伤神经保护的研究提供新的实验方法.方法出生后5d的ICR种小鼠60只,随机分为IA组和生理盐水(normal sodium,NS)组.IA组脑内注射神经兴奋毒素IA后随机分为IA1(24h)和IA2(120h)组,NS组脑内注射等量生理盐水后随机分为NS1(24h)组和NS2(120h)组.分别于脑内注射后24h和120h断头处死小鼠,观察脑组织病理学,计算各组脑组织的损伤直径.结果IA组小鼠脑组织病理组织切片显示明显的脑白质区囊性病变.IA1组脑损伤直径为(516.7±123.3)μm,IA2组脑损伤直径为(1400±153.2)μm;NS1组脑损伤直径为(250.7±119.5)μm,NS2组脑损伤直径为(382±118.8)μm,IA组脑损伤直径明显大于NS组(P<0.01).结论脑内注射神经兴奋毒素鹅膏蕈氨酸能够造成小鼠明显的脑室周围白质区囊性病变。Objectives To provide a model of the white matter damage in neonatal mice brain through in- tracerebral injection of ibotenate and provide a new experimental method for neonatal excitotoxic white matter dam- age protection. Methods Sixty 5-day-old ICR neonatal mice were randomly divided into two groups: ibotenate acid (IA) control (n = 30) and normal sodium (NS) control (n = 30). After intracerebral injection Of ibote- nate in group IA, the pups were divided in two sub-groups at random, group IA1 and group IA2. Similarity, after intraceberal injection of normal sodium in group NS, the pups were divided into two sub-group, group NS1 and group NS2. 24 hours after intracerebral injection, all pups of group IA1 and group NSI were decapitated, and their brains were taken for histological and pathological observation. 120 hours after intracerebral injection, all pups of group IA2 and group NS2 were also decapitated, and their brains were taken for histological and pathological observation. Then we calculated the diameter of the brain damage. Results Cystic lesions of white matter were observed in pathological slides of group IA. The diameter of brain damage in group IA1 was (516.7 ± 123.3) μm,group IA2 was (1400 ± 153.2) μm; and the group NS1 was (250.7 ± 119.5) μm, group NS2 was (382 ± 118.8) μm. The diameter of brain damage in group IA was longer than group NS (P 〈 0.01 ). Gonclusion Intracerebral injection of ibotenate can cause cystic lesions of white matter andinduce a model of the excitotoxic brain damage in neonatal mice.
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