OBJECTIVE： To study the effects of erythropoietin （EPO） on cognitive function of neonatal rats with hypoxic- ischemic brain injury （HIBI）， and the regulation mechanism of related PARP-1/AIF signaling pathway. METHODS： SD neonatal rats were randomly divided into sham operation group （Sham group）， model group （HIBI group） and EPO intervention group （EPO group）， with 22 rats in each group. HIBI model was induced by Rice method in HIBI group and EPO group， and rats in sham group received suturing after cutting without hypoxic-ischemic treatment. After modeling， rats in EPO group was given Erythropoietin injection intraperitoneally each day， 5 000 IU/kg，for consecutive 14 d. Rats in Sham group and HIBI group were given constant volume of normal saline intraperitoneally. Cerebral tissue of rats was collected， and TTC staining was used to detect cerebral infraction. Neuronal apoptosis in hippocampal CA1 region was detected by TUNEL method. The expression of PARP-1，AIF and Bax protein in hippocampal CA1 region was detected by Western blot. Morris water maze was used to examine the spatial learning and memory abilities of rats. RESULTS： Compared with Sham group， the cerebral infarction area of rats in HIBI group was increased significantly； the number of TUNEL positive apoptosis cells in neuron of hippocampal CA1 region was increased significantly； the protein expression levels of PARP-1， AIF and Bax were increased significantly； in Morris water maze experiment， the escape latency of rats was prolonged significantly， while the index of crossing the platform was decreased significantly， with statistical significance （P＜0.05）. Compared with HIBI group， cerebral infraction area of rats in EPO group was decreased significantly； the number of TUNEL positive apoptosis cells in neuron of hippocampal CA1 region was decreased significantly； the protein expression levels of PARP-1， AIF and Bax were decreased significantly； in Morris water maze experiment， the escape latency of rats was shortened significantly， while the index of crossing the platform was increased significantly， with statistical significance （P＜0.05）. CONCLUSIONS：EPO can significantly inhibit HIBI-induced neuron apoptosis of rats so as to play protective effect on cerebral tissue， and promote the recovery of cognitive function， the mechanism of which may be associated with inhibiting apoptosis PARP-1/AIF signaling pathway.