摘要
目的探讨新生动物缺氧缺血性脑病（ＨＩＥ）中脑细胞损伤时是否存在细胞凋亡（ａｐｏｐｔｏｓｉｓ，Ａｐｏ），探索在ＨＩＥ发病机制中缺氧、缺血两因素与凋亡是否存在相关关系。方法通过建立ＨＩＥ标准化动物模型，应用ＨＥ染色、电镜、组织切片原位末端标记技术（Ｔｕｎｅｌ）等手段，分别对缺氧、缺血、缺氧缺血和对照四组动物的实验侧脑皮质、海马中凋亡细胞的形态、特点、密度进行观察和比较。结果光镜和电镜显示细胞皱缩、染色质断片、Ａｐｏ小体；原位标记显示在脑皮质、海马回、丘脑均有裂解的ＤＮＡ存在；四组凋亡指数：脑皮质区域、海马区域两因素及其交互作用均有统计学意义（Ｆ＝３５６．３４，Ｐ＜０．０１，Ｆ＝４１７．４４，Ｐ＜０．０１）。结论缺氧、缺血两因素均可引起脑细胞凋亡，联合作用与脑细胞凋亡有明显相关性，在ＨＩＥ中细胞死亡不仅是传统的坏死结果，而且存在着凋亡机制的作用。
Objective To determine whether or not apoptosis occurs in neonatal hypoxiaischemia (HIE), and assess the relationship between apoptosis and hypoxia or ischemia. Method Using HE staining and electronmicroscope technique, terminal deoxynuleotidyl transferasemediated dUTP nick end labelling (Tunel), the authors observed the histological features, densities of apoptotic cells in the cerebral cortex, hippocampus at ipsilateral hemisphere in neonatal rat models of hypoxia, ischemia, hypoxiaischemia, and normal controls. Result Light and electron microscopy exhibited cell shrinkage, internucleosomal cleavage, apoptosis bodies in rats with HIE. Cells containing cleaved DNA were also identified by in situ labelling in the cortex, hippocampus of the ipsilateral hemisphere. Quantitative analysis of the groups showed that apoptosis occurred in the cortex (F=356.34, P<0.01) and hippocampus (F=417.44, P<0.01) following HIE. Conclusion Cerebral hypoxia and ischemia may induce apoptosis. The cell death in HIE may result not only from traditional necrosis, but also from apoptosis.
出处
《中华儿科杂志》
CAS
CSCD
北大核心
1998年第7期408-411,共4页
Chinese Journal of Pediatrics
基金
铁道部科技基金
