Nerve protective effect of rhTPO and G-CSF on hypoxic ischemic brain damage in rats

Objective:To observe the protection effect of rhTPO and granulocyte colony stimulating factor(G-CSFi 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 of 120 newborn SD rats aging 7 d were randomly divided into control group,model group,TPO group and G-CSF group,using the method of blockingleft carotid artery to establish HIBD model.The left carotid artery was only seperated rather than blocked in the control group;after modeling,saline injection,rhTPO treatment and G-CSF treatment were adopted in the model group,TPO group and C-CSF group respectively.Then 10rats of 4 groups were executed at Day 3,7,14 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 and G-CSF group were significantly higher than that of control group at corresponding time point(P<0.05).Injured brain mass of TPO group and G-CSF group were significantly lower than that of model group(P<0.05),and with the increase of age,more significant increasing trend.At Day 3 after modeling,the expression of nestin positive cells in cerebral cortex of model group,TPO group and G-CSF gnmp increased significantly than that of control group{P<0.05);nestin positive cells of G-CSF group outnumbered TPO group significantly(P<0.05).Conclusions:The early TPO,G-CSF treatment of HIBD rats can improve brain function after hypoxia ischemia by neural protection.G-CSF can promote the differentiation of neural cells proliferation,and reduee degeneration and necrosis of nerve cells.

Objective:To observe the protection effect of rhTPO and granulocyte colony stimulating factor(G-CSFi 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 of 120 newborn SD rats aging 7 d were randomly divided into control group,model group,TPO group and G-CSF group,using the method of blockingleft carotid artery to establish HIBD model.The left carotid artery was only seperated rather than blocked in the control group;after modeling,saline injection,rhTPO treatment and G-CSF treatment were adopted in the model group,TPO group and C-CSF group respectively.Then 10rats of 4 groups were executed at Day 3,7,14 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 and G-CSF group were significantly higher than that of control group at corresponding time point(P&lt;0.05).Injured brain mass of TPO group and G-CSF group were significantly lower than that of model group(P&lt;0.05),and with the increase of age,more significant increasing trend.At Day 3 after modeling,the expression of nestin positive cells in cerebral cortex of model group,TPO group and G-CSF gnmp increased significantly than that of control group{P&lt;0.05);nestin positive cells of G-CSF group outnumbered TPO group significantly(P&lt;0.05).Conclusions:The early TPO,G-CSF treatment of HIBD rats can improve brain function after hypoxia ischemia by neural protection.G-CSF can promote the differentiation of neural cells proliferation,and reduee degeneration and necrosis of nerve cells.