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Chinese Journal of Tissue Engineering Research ; (53): 6837-6840, 2010.
Artigo em Chinês | WPRIM | ID: wpr-402327

RESUMO

BACKGROUND: Nestin is a specific antigen of neural stem cells which widely expressed in lesion of nervous system and brain regeneration.Thus,nestin expression is commonly used to assess whether lesion or damage of the nervous system can promote neural regeneration.OBJECTIVE: To investigate the effects of erythropoietin(EPO)on nestin expression in neural stem cells after hypoxia-ischemia brain damage(HIBD)in neonatal rats from the angles of neural regeneration and activation of neural stem cells.METHODS: HIBD model was established by ligation of the right common carotid artery along with 2-hour 8% hypoxia exposure in neonatal rats.The control group was not subjected to hypoxia-ischemia,and the right common carotid artery was dissociated.The treatment group received an intraperitoneal injection of recombinant human erythropoietin(rh-Epo,5 000 IU/kg)once a day for three days after hypoxia/ischemia,while the two other groups intraperitoneally received normal saline at the same time.In each group,rats were randomly executed immediately,at 4,7,14 days after operation(n = 8).The nestin expression in hippocampal dentate gyrus region was examined by immunohistochemical staining and image quantitative analysis respectively.RESULTS AND CONCLUSION: The number of nestin-positive cells was significantly increased in HIBD group compared to control group at all time points(P < 0.05),and it was also significantly increased in treatment group than the other two groups at all time points(P < 0.05).The numbers of nestin-positive cells in hippocampal dentate gyrus region were significantly increased,and peaked on day 7 after operation in the three groups.The results showed that exogenous rh-Epo could enhance the expression of nestin in hippocampal dentate gyrus region of neonatal rats with HIBD,and promote the proliferation of neural stem cells,rh-Epo plays an important role in the regeneration and repair of neurocytes damaged by hypoxia-ischemia.

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