【摘要】 目的研究人脑梗死后海马β-淀粉样蛋白1-40(Aβ1-40)、β-淀粉样蛋白1-42(Aβ1-42)和载脂蛋白E(ApoE)在海马神经元中表达的时空变化。方法选取因脑梗死尸检脑标本43例以及因其它疾病死亡(非脑缺血)的尸检脑标本6例(对照组),应用HE染色方法观察海马神经元形态变化,应用免疫组化方法检测人脑梗死后这3种蛋白分别在海马CA1和CA3区神经元中的表达情况。结果在对照组和梗死组中,这3种蛋白在神经元中均有表达,且均主要表达于胞浆。Aβ1-40和Aβ1-42的表达于梗死后均迅速增加,ApoE的表达在梗死后亦增加。结论人脑梗死后海马CA1和CA3区Aβ1-40、Aβ1-42和ApoE在海马CA1和CA3区神经元中的表达均增加,脑梗死可能导致了这3种蛋白的聚集,同时Aβ和ApoE表达的上调可能部分解释了脑梗死在AD的发病机制中所起的作用。更多还原

【Abstract】 Objective To investigate the spatiotemporalchanges of Aβ1-40,Aβ1-42 and ApoE expression in the human hippocampus following cerebral infarction. Methods 43 human brains with focal cerebral infarction and 6 brains from patients died of other diseases without cerebral ischemia obtained at autopsy were investigated. Morphological changes were analyzed by observing HE staining,and the postischemic time course of neuronal Aβ1-40,Aβ1-42 and ApoE immunoreactivites in the hippocampal CA₁ and CA₃ regions were examined respectively. Results In neurons of the CA₁ and CA₃ regions,the immunoreactivities of Aβ1-40,Aβ1-42 and ApoE,all of which were predominantly present in the cytoplasm,were observed in both control and ischemic groups. The accumulation of both Aβ1-40 and Aβ1-42 were increased dramatically and consistently after cerebral infarction. Neuronal ApoE immunoreactivity was also significantly increased in all the ischemic group compared with controls. Conclusion The most likely stimulus for increasing of Aβ1-40,Aβ1-42 and ApoE immunoreactivities in the CA₁ and CA₃ neurons are ischemic conditions,and their upregulation,in turn,may partly explain the contribution of cerebral infarction to the pathogenesis of Alzheimer’s disease.更多还原