RESUMO
AIM: To study the neuroprotective effect and possible mechanism of ganglioside GM1 on neonatal rats with hypoxic ischemic encephalopathy (HIE). METHODS: A rat model of neonatal HIE was established, then the pathological changes and expressions of glutamate and EAAC1 glutamate transporter in the brain tissues were investigated in different periods after hypoxia ischemia (HI) and the subsequent changes of the above results after GM1 administrated were studied too. RESULTS: The damages of the brain by exposed to HI were alleviated remarkably after GM1 administrated. The levels of glutamate neuron expressions in the brain tissue decreased after HI but EAAC1 increased. GM1 could partly prevent glutamate neuron reduction induced by HI and increase EAAC1 expression. CONCLUSION: GM1 may have some protective effects on glutamate neuron in neonatal HIE, and the possible mechanism is related to the partial increasing of EAAC1 expression.