| Neonatal hypoxic and ischemic encephalopathy (HIE) is a nerve system injured disease which is caused by all kinds of hypoxic and ischemic (HI) factors at perinatal period.It has become the major research field all over the world in the scope of perinatal medicine due to its high mortality, its sequelae (such as amentia, brain palsy, epilepsy and so on). It is one of common reason which causes newborn nerve system injured. The pathogenesis of HIE is extremely complicated, so the mechanism of brain damage has not yet been understood. In the past, the studies of the pathogenesis of HIE were mainly focused on neurons. Recently, with the study of glial cells gradually deepened, it were found that glial cells are abnormally active, appear complicated change at the molecular level and bidirectionally effect on the neurons after HI in the brain. The plasticity and response of glial cells to microenvironment differ at the different development phases. The plasticity of Newborn glial cells is higher than that of adult ones, but the sensitive of Newborn glial cells to HI is much higher than that of adult one. In the past the studies of the function of the glial cells in HIBD was focused on adult rats, and more focused on astrocyte, but the studies of microglia and oligodendrocyte were little. The general studies of the change of three kinds of glial cells in neonatal rats or newborn after HIBD have not yet been reported. So the studies of the intricate change of different glial cells in the network of colloid neonatal rats and newborn after HIBD and the relationship between glial cells change and neurons will lay a foundation for further exploring the function of glial cells in the pathogenesis of newborn HIE and thereout breaking a new treatment pathway. There are three parts in this study. In the first part, the neurons apoptosis and the change of glial cells in neonatal HIE and the relationships between nerve pathology and clinical were observed; In the second part, the relationship between glial cells change and neurons apoptosis were systemically observed by experimental hypoxic-ischemic brain damage in neonatal rats; In the third part, it was observed that topamax had or not the neuroprotective effect on experimental neonatal hypoxic-ischemic brain damage rats. In this study, the pathological brain specimens of 25 newborn who died of HIE were observed macroscopically and microscopically. HE staining was performed to primarily observed the change of brain tissue, and immunochemistry staining and in situ end labeling TUNEL methods were used to attempte to observe the neurons apoptosis and the change of glial cells in the condition of HI. Thereby the occurrence of HIE, course of disease, newborn degree of maturity and nerve pathology were further synthetically analysed in order to more directly and more precisely observe the discipline of nerve pathological change in newborn HIE. It will favor the further study of pathogenesis of newborn suffering from HIE in order to give the reference for clinic. But there is certain limitation in the observation and study by pathological specimens of human newborn HIE, for instance, the dead newborn HIE are all at severe degree so that we can not compare the discipline of change of glial cells in newborn HIE at different degree. Furthermore, because Newborn HIE are dead shortly after birth, it unable to observe the change of glial cells at different time spots, especially the newborn's anaphase change. Otherwise clinical factors are intricate so that it is difficult to control them. It is unable to summarize the deep-seated discipline in short time, hence the further study was performed by animal experiment in this paper.The fetus's intrauterine asphyxia and natal asphyxia are the main reasons which cause newborn HIE, therefore the perinatal period HIBD animal model was established by the ligation of both uterine arteries of full-term pregnant rats in this study. Immunochemistry staining was performed to label the glial cells (the astrocyte was la...
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