OBJECTIVETo investigate the effects of erythropoietin (EPO) on the neuronal proliferation and apoptosis in neonatal rats after infection-induced brain injury and the neuroprotective mechanism of EPO in neonatal rats with infection-induced brain injury.

METHODSTwenty-six two-day-old neonatal rats were randomly divided into 3 groups: control group (intraperitoneally given an equal volume of normal saline), lipopolysaccharide (LPS) group (intraperitoneally given LPS 0.6 mg/kg), and EPO group (intraperitoneally given LPS 0.6 mg/kg and EPO 5 000 U/kg). These groups were injected with respective drugs for 5 consecutive days. Meanwhile, each group was intraperitoneally injected with 5-bromo-2'-deoxyuridine (BrdU) (50 mg/kg) once a day for 5 consecutive days. The expression of BrdU and cleaved Caspase-3 in the hippocampal dentate gyrus was detected by immunohistochemistry at 24 hours after the last injection.

RESULTSThe number of neuronal cells in the hippocampal dentate gyrus in the LPS and EPO groups was significantly greater than in the control group (P<0.05), but there was no significant difference between the LPS and EPO groups. The EPO group had a significantly higher number of BrdU-positive cells in the subgranular zone of hippocampal dentate gyrus than the LPS group (51±9 vs 29±6; P<0.05), but a significantly lower number of BrdU-positive cells than the control group (51±9 vs 67±12; P<0.05). The EPO group had a significantly lower number of cleaved Caspase-3-positive cells in the subgranular zone of hippocampal dentate gyrus than the LPS group (27.9±1.5 vs 34.0±1.3; P<0.05), but a significantly higher number of cleaved Caspase-3-positive cells than the control group (27.9±1.5 vs 21.0±1.7; P<0.05).

CONCLUSIONSEPO can promote hippocampal neuronal proliferation and reduce neuronal apoptosis in neonatal rats after infection-induced brain injury.