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[Objective] analog birth asphyxia, hypoxic-model to study the expression of hypoxia on neonatal rat brain-derived differentiation factor (NeuroD) and apoptosis and nerve regeneration impact neonatal perinatal asphyxia caused by hypoxic-ischemic encephalopathy prevention provide experimental evidence. [Method] reference to Grojean method, newborn rats were briefly placed in 100% nitrogen environment, the establishment of the model of birth asphyxia. Neurological behavior observation, HE staining and transmission electron microscopy of brain tissue pathological changes, to be evaluated in animal models. The animals were randomly divided into control group, hypoxia 10min, hypoxia 20min group, using frozen section immunofluorescence, Western blot was used to detect the change of the the NeuroD expression level of. The animals were randomly divided into control group, hypoxia group 20min subfractions 13d, 20d, 27D three time points drawn, frozen section immunofluorescence NeuroD paraffin sections immunohistochemical detection of BrdU expression changes. Another sub-component 6d, 20d two time points, cell apoptosis was detected by TUNEL method. [Results] 1. Anoxia neonatal rat systemic cyanosis, unconsciousness and other neurobehavioral abnormalities. HE staining hypoxia 10min hippocampal CA1 region of the nerve cell swelling, increased hypoxia 20min nerve cell damage. The ultrastructure Show hypoxia 10 min early manifestation of neuronal apoptosis: nuclear chromatin margination, formation of secondary lysosomes. Microvascular endothelial cells, pericytes vacuolar degeneration occurs. 20min after hypoxia visible neuronal necrosis, nuclear fusion, cell blurred. Perimicrovascular Star glia feet, swollen cell processes. Immunofluorescence results show that in the cerebral cortex and hippocampus dentate gyrus visible NeuroD expression by Western blot analysis also with hypoxic extension of time NeuroD expression was significantly increased (P lt; 0.01) 3 immunofluorescence / group, hypoxia 20min 13d, 27D NeuroD / BrdU in the hippocampal CA1 region / SVZ of expression were higher than that in the control group (P <0.05), and in 20D the expression of the highest (P <0.01 ). TUNEL assay 6d 20min after hypoxia in the hippocampal CA1 region of apoptotic cells was significantly higher than that in the control group (P <0.01), and 20d apoptotic cells positive rate with the control group showed no significant difference. [Conclusion] 1. Neonatal rat briefly in 100% nitrogen environment can be established with human neonatal ischemic hypoxic brain damage in neonatal rats with birth asphyxia HIE model. Transient hypoxia can cause the NeuroD expression level of increase the expression sites mainly in the cerebral cortex, hippocampus, SVZ of neural stem / precursor cells enclave. Hypoxia causes delayed apoptosis of neuronal loss, can induce cell proliferation and neuronal differentiation, the trigger neurogenesis, to carry out the compensatory repair and reconstruction of the nerve function of damaged brain tissue.
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