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

Abstract

ObjectiveTo 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. MethodsA 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 G-CSF group respectively. Then 10 rats 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. ResultsInjured 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 group increased significantly than that of control group (P<0.05); nestin positive cells of G-CSF group outnumbered TPO group significantly (P<0.05). ConclusionsThe 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 reduce degeneration and necrosis of nerve cells.