To investigate the protective effects of testosterone propionate (TP) on hypoxic-ischemic brain damage (HIBD) neonatal rat brain by observing oligodendrocyte myelin glycoprotein (OMgp) expression in the cortex and hippocampus after HIBD. Materials and methods: Rats were randomly divided into 3 groups: TP pretreatment, HIBD control, and a sham treatment group. Rats 7 days old from the TP group and HIBD control group were subjected to HIBD, and OMgp expression in the hippocampus and cerebral cortex of the different doses and groups was observed after hypoxic-ischemic induction at 24 h, 48 h, 72 h, 7 days, and 14 days. Results: The OMgp expression in the brain tissue of the HIBD control group was significantly higher than that of the sham group at the same point in time (P < 0.01). After intervention with TP, OMgp expression in the hippocampus and cortex (30 mg/kg and 120 mg/kg) was significantly reduced compared with the HIBD control group (P < 0.01). Conclusion: OMgp expression in neonatal rat brain tissues was increased after HIBD; OMgp overexpression was inhibited after intervention with TP. Therefore, androgen may play an important role in removing inhibition of OMgp on axon growth, and thus promote axonal regeneration, playing a protective role in the brain.

To investigate the protective effects of testosterone propionate (TP) on hypoxic-ischemic brain damage (HIBD) neonatal rat brain by observing oligodendrocyte myelin glycoprotein (OMgp) expression in the cortex and hippocampus after HIBD. Materials and methods: Rats were randomly divided into 3 groups: TP pretreatment, HIBD control, and a sham treatment group. Rats 7 days old from the TP group and HIBD control group were subjected to HIBD, and OMgp expression in the hippocampus and cerebral cortex of the different doses and groups was observed after hypoxic-ischemic induction at 24 h, 48 h, 72 h, 7 days, and 14 days. Results: The OMgp expression in the brain tissue of the HIBD control group was significantly higher than that of the sham group at the same point in time (P < 0.01). After intervention with TP, OMgp expression in the hippocampus and cortex (30 mg/kg and 120 mg/kg) was significantly reduced compared with the HIBD control group (P < 0.01). Conclusion: OMgp expression in neonatal rat brain tissues was increased after HIBD; OMgp overexpression was inhibited after intervention with TP. Therefore, androgen may play an important role in removing inhibition of OMgp on axon growth, and thus promote axonal regeneration, playing a protective role in the brain.