Objective: To 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.
Methods: Twenty-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.
Results: The 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).
Conclusions: EPO can promote hippocampal neuronal proliferation and reduce neuronal apoptosis in neonatal rats after infection-induced brain injury.