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Objective:To observe the protection effect of rhTPO and granulocyte colony stimulating factor (G-CSF) on brain nerve after hypoxic ischemic brain damage(HIBD) in neonatal rats, exploring new ways for the laboratory basis of treatment for hypoxic ischemic encephalopathy, and provide for possible.Methods:A total of120 newbSD rats aging7 d were randomly divided into control group, model group,TPO group andG-CSF group, using the method of blockingleft carotid artery to establishHIBD model.The left carotid artery was only seperated rather than blocked in the control group; after modeling, saline injection, rhTPO treatment andG-CSF treatment were adopted in the model group,TPO group andG-CSF group respectively.Then10 rats of4 groups were executed atDay3,7,14 after modeling, brain tissue was extracted to observe the brain damage;Immunohistochemical method was used to observe the histopathological changes of brain tissue and changes of nest protein(nestin) expression.Results:Injured brain mass of model group,TPO group andG-CSF group were significantly higher than that of control group at corresponding time point(P<0.05).Injured brain mass ofTPO group andG-CSF group were significantly lower than that of model group(P<0.05), and with the increase of age, more significant increasing trend.AtDay3 after modeling, the expression of nestin positive cells in cerebral cortex of model group,TPO group andG-CSF group increased significantly than that of control group(P<0.05); nestin positive cells ofG-CSF group outnumberedTPO group significantly (P<0.05).Conclusions:The earlyTPO,G-CSF treatment ofHIBD rats can improve brain function after hypoxia ischemia by neural protection.G-CSF can promote the differentiation of neural cells proliferation, and reduce degeneration and necrosis of nerve cells.