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人脑缺血后神经元损伤与死亡相关因素的关系 被引量:1

Ischemic neuron injury in human hippocampusand and its correlation to Caspase-3,MAP-2 and Tubulin
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摘要 目的 研究人脑局灶性缺血后海马神经元损伤形式及其与死亡相关因素胱冬酶 3(Caspase 3) ,微管相关蛋白 2 (MAP 2 ) ,微管蛋白 (Tubulin)之间的关系。方法 选取 4 8例因脑梗死而死亡的尸检脑标本 ,应用HE染色、Caspase 3mRNA原位杂交、末端脱氧核糖核酸转移酶介导的缺口末端标记 (TUNEL)法、MAP 2和Tubulin免疫组织化学染色 ,观察局灶性脑缺血时海马CA1区神经元损伤变化。结果 海马CA1区 ,Caspase 3mRNA原位杂交阳性表达始于 8h ,2 4h达高峰 ;二者均在 72~ 96h后呈明显下降趋势。缺血 2 4h ,可检测到TUNEL阳性细胞。早在 8h即可检测到明显的MAP 2、Tubulin免疫活性下降 ,之后持续下降 ,至 72h几乎无阳性表达细胞。 8~ 16h ,受损神经元形态基本正常 ;2 4~ 72h细胞凋亡特征明显 ;96h后 ,几乎所有神经元形态均呈现严重病理变化。结论 人脑局灶性缺血后海马神经元发生一系列形态学变化 ,72h前损伤神经元呈现凋亡特征 ,其演变规律与凋亡促进因子Caspase 3有显著相关性 ;96h后 ,受损神经元呈现胀亡特征 ,与Caspase 3无明显相关性。无论神经元发生何种形式死亡 ,其MAP Objective To investigate the change of ischemic neuronal injury and its correlation to Caspase-3,microtubule-associated protein 2(MAP-2) and Tubulin post-ischemia in human hippocampus.Methods We stained sections with hematoxyline/eosin and used Caspase-3,terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate-biotin nick-end labeling (TUNEL),MAP-2 as markers to observe changes of hippocampal CA1 neurons in post-mortem specimens from 48 patients,who were died of cerebral infarction.Results In the CA1 sector of hippocampus,Caspase-3 mRNA was detectable at 8h,reached a maximum at 24h,faded at 72h.TUNEL-positive cells were detectable at 24h,markedly increased at 48~72h.The loss of MAP-2 was obviously detected at 4h,progressed significantly between 24 and 72h;MAP-2 and Tubulin immunoreactivity was barely detectable at 72h.Before 72h,the Caspase-3 evolution was in parallel with both the up-regulation of TUNEL and the loss of MAP-2.At 4~16h,most neurons in hippocampal CA1 areas had relatively normal morphology;at 24~72h,neurons showed apoptotic morphology;after 96h,most cells showed significantly pathological morphology.Conclusion Before 72h,there is a time-dependent evolution of neuronal apoptosis after hippocampal ischemia in human brain,which is characterized by its close correspondence to Caspase-3.After 96h,some cells show oncotic morphology,which have no correlation to Caspase-3.MAP-2 and Tubulin continously degrade in a time-dependent manner.
出处 《哈尔滨医科大学学报》 CAS 北大核心 2005年第1期10-13,F004,共5页 Journal of Harbin Medical University
基金 国家自然科学基金资助项目 ( 3 0 2 70 480 ) 黑龙江省自然科学基金项目 (D0 2 0 3 )
关键词 脑缺血 神经元损伤 病理学 cerebral ischemia neuron injury pathology
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