Expression of brain-derived erythropoietin in hippocampus of neonatal rats with hypoxic-ischemic brain damage

Objective To examine the expression of brain-derived erythropoietin in the hippocampus of neonatal rats with hypoxic-ischemic brain damage (HIBD) , and explore the mechanism of neurogenesis in the hippocampus triggered by endogenous risk factors after HIBD. Methods One hundred and ninety-two 7-day-old Sprague-Dawley (SD) rats were studied: 96 underwent immunohistochemical staining, and 96 used for Western blot analysis. All the SD rats were randomly divided into three groups: control (C), hypoxia (H) and hypoxia-ischemia (HI) groups. In 64 rats (13 to 19 g of body weight) left common carotid artery was ligated, then exposed to hypoxic condition to establish the model of neonatal HIBD. Each group was assessed at 1 h, 6 h, 16 h, 1 d, 3 d and 7 d time points. Four rats from C group, 4 rats from H group, and 8 rats of HI group were examined at every time point. Immunohistochemical staining and Western blot were used to identify the expression of brain-derived erythropoietin in the hippocampal CA1 at every time point after HIBD. Results There was a significant difference in the expression of brain-derived erythropoietin among three groups, and most significant changes were found in HI group. The changes at different time points in C group were not significant. The expression changed with time in H and HI groups: first detected in hippocampal CA1 region at 1 h after HIBD, reached peak level at 16 h after HIBD, and then decreased after that. Conclusions The expression of brain-derived erythropoietin increased early after hypoxia. Hypoxia, overexpression of erythropoietin at that time was probably one of endogenous factors involved in the neurogenesis in neonatal hippocampus after HIBD.