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作 者:蒋犁[1,2,3] 汤云珍[1,2,3] 黄晓明[1,2,3] 陈平圣[1,2,3] 胡向阳[1,2,3]
机构地区:[1]南京铁道医学院儿科实验室 [2]南京铁道医学院医学科学研究所 [3]南京铁道医学院病理学教研室
出 处:《南京铁道医学院学报》1998年第3期151-154,共4页Journal of Nanjing Railway Medical College
基 金:铁道部科技基金
摘 要:目的:探讨新生儿缺氧缺血性脑病(HIE)中海马迟发性神经元死亡现象,研究其凋亡的作用机理。方法:通过HIE的动物模型,应用DNA电泳、电镜、原位末端标记技术等手段,分别对缺氧3h完成后1、4、18、24、40、72h及7d组和对照组海马凋亡细胞形态、密度、时间进行观察比较。结果:光镜、电镜显示细胞皱缩、染色质边集、出现凋亡小体,DNA电泳图谱显示梯状形态,原位标记显示海马各区标记阳性的细胞,定量比较显示HIE后40h点海马细胞凋亡最明显,其中CA1区持续至7d以后。结论:在HIE中细胞死亡存在着凋亡作用;Objective:To study the potential role of apoptosis and delayed cell death of hippocampus following neonatal hypoxia-ischemia (HIE).Method:establishing the animal model of HIE and observing cell apoptosis in the hippocampus after permanent ischemia 1,4,18,24,40,72 h,7 d with control group. Using electrophoresis, and electron-microscope, terminal deoxynuleotidyl transferase nick end labeling(Tunel) technique,the shape,density and time of the cell death have been observed and compared in the apoptotic cells.Result:The morphologic changes of cell apoptosis including cell shrinkage,chromatic condensation and apoptotic bodies, ladder electrophoresis,DNA fragmentation were found. The peak of cell apoptosis was at 40h after hypoxia-ischemia.It was maily located in CA 1 region.Conclusion:The cell death of HIE was caused by necorosis and apoptosis with showing delayed neuronal death in the hippocampus of immature brain after HIE.
分 类 号:R722.120.2[医药卫生—儿科]
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