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脑梗死后海马神经元β-APP及其产物与ApoE的表达

Expression of β-Amyloid Precursor Protein,β-Amyloid Protein and Apolipoprotein E in Neurons of Hippocampus after Cerebral Infarction
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摘要 目的:应用常规HE染色和免疫组织化学染色方法,观察人脑梗死后海马CA1区和CA3区神经元中β-APP、Aβ1-40、Aβ1-42及ApoE的表达,探讨它们表达变化的时间规律,以期对临床治疗提供可靠的实验资料。方法:分脑缺血组和对照组,脑缺血组按缺血时间分为缺血2h-6h组、7h-24h组、25h-48 h组、49h-72h组、73h-96h组、97h-144 h组和145h-168 h组。采用HE染色方法观察神经细胞损伤情况;免疫组织化学染色检测β-APP、Aβ1-40、Aβ1-42与ApoE在尸检脑标本海马CA1区、CA3区神经元的表达,在显微镜下对免疫组织化学染色阳性细胞计数,实验结果应用SPSS12.0统计软件进行分析。结果:与对照组相比,Aβ1-40的表达在缺血2h后明显增加,73h-96 h达高峰,以后有所回落,但仍高于对照组;β-APP在缺血2 h-6 h表达呈峰值,49 h-96h呈现第二次高峰,96 h以后下降,但仍高于对照组;于缺血24 h后,β-APP和Aβ1-40的增加呈显著的正相关。缺血2 h后,Aβ1-42表达开始增加,25 h-48 h达高峰;缺血6 h后,ApoE表达开始增加,但97 h-144 h为高峰期。结论:人脑梗死后β-APP、Aβ-40和Aβ1-42表达增加,它们可协同加重脑缺血性损伤;而ApoE脑保护作用可能增强。 Objective: To observe the expression of β-APP, Aβ1-40, Aβ1-42 and ApoE in the neurons in the hippocampus CA1 and CA3 regions after human cerebral infarction so as to provide reliable experimental data for clinical application. Methods: 48 (male=28, female=20) patients' autopsy specimens, clinically diagnosed cerebral infarction, were selected as cerebral ischemia group which was further divided into 7 groups according to ischemia time; 5 (male=5) patients' autopsy specimens, died of other diseases except cerebral infarction, were selected as control group. The injury of nerve cells was observed by HE staining; and the expression of β-APP, Aβ1-40, Aβ1-42 and ApoE was determined by immunohistochemistry in the neurons in the hippocampus CA1 and CA3 regions in the autopsy cerebral specimens. All of the experiments were statistically analyzed by the SPSS 12.0 for windows software. Results: Compared to control group, there was a significant direct correlation between the increase of the β-APP and Aβ1-40 24h after cerebral ischemia; the expression of Aβ1-42 began to increase 2h after ischemia and peaked at 25h-48h; the expression of ApoE began to increase 6h after ischemia but peaked at 97h-144h. Conclusions: The expression of the β-APP, Aβ1-40 and Aβ1-42 were up-regulated after cerebral infarction, which might aggravate cerebral ischemia. Meanwhile, the effect of ApoE on brain protection may be increased.
出处 《现代生物医学进展》 CAS 2007年第10期1454-1457,共4页 Progress in Modern Biomedicine
基金 国家自然科学基金(30270480)
关键词 Β淀粉样蛋白 Β淀粉样前体蛋白 载脂蛋白E 脑梗死 Beta-amyloid protein Beta-amyloid precursor protein Apolipoprotein E Human Cerebral infarction
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参考文献13

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