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作 者:穆永茂[1] 臧贺川[1] 刘和亮[2] 李世英[1] 冯云[1]
机构地区:[1]华北煤炭医学院附属医院神经内科,唐山063000 [2]华北煤炭医学院中心实验室
出 处:《脑与神经疾病杂志》2008年第4期379-382,共4页Journal of Brain and Nervous Diseases
摘 要:目的:研究急性一氧化碳中毒大鼠迟发性脑病模型中脑红蛋白(NGB)在额叶皮质和海马区的表达变化情况。方法:腹腔注射纯CO制备急性一氧化碳中毒与一氧化碳中毒迟发性脑病的大鼠模型。检测大鼠大脑皮质及海马区细胞的脑红蛋白的表达情况。结果:急性一氧化碳中毒后大鼠额叶皮质的NGB蛋白表达于损伤后第1天上调,以后逐渐降低至染毒后21d;而海马区NGB表达降低并呈持续减少的趋势,至染毒后21d最低;与对照组相比差异均有统计学意义(p<0.01)。病理学检测显示海马区神经细胞损伤程度较额叶皮质严重。结论:(1)脑不同部位对一氧化碳中毒的耐受性差异可能与NGB的表达有关。(2)NGB的表达下调可能与一氧化碳中毒迟发性脑病的发生与发展有关。Objective:To observe the dynamic changes of neurogolbin(NGB) expression in delayed encephalopathy rat with of acute carbon monoxide poisoning.Methods:Delayed encephalopathy rat model of acute carbon monoxide poisoning was induced by ip injected with CO repeatedly,then the brains of the CO exposed rats were taken after injection of CO 1、3、7、14 and 21d.The NGB expression in cerebral cortex and hippocampus of each group was measured with immunohistochemical methods coupled with computer-assisted image analysis.Results:The changes in NGB expression were different in cerebral cortex and in hippocampus.NGB protein was up-regulated from 1d after injection of CO in cerebral cortex whereas it was down-regulated in hippocampus and the expression was the lowest at 21d after CO exposure,it was lower in the CO-exposed group than in the normal group(p〈0.01).Conclusion:(1) The different expressions of NGB in cerebral cortex and hippocampus are suggestive of different compensatory and repair mechanisms.(2) The low expression of endogenous NGB in the brain after acute carbon monoxide may be associated with the occurrence and development of the delayed encephalopathy.
关 键 词:一氧化碳中毒 急性一氧化碳中毒迟发性脑病 脑红蛋白
分 类 号:R747.8[医药卫生—神经病学与精神病学]
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