To test the hypothesis that Gln may regulate the MKP-1/MAPK pathway and cause a decrease in oxidative stress, inflammation, and apoptosis, thereby preventing brain damage, learning difficulties and memory dysfunction caused by hyp-induced injury, in this study we investigated the protective role of Gln in hyp-induced brain injury in neonatal rats and its association with the MKP-1/MAPK signaling pathway using a neonatal rat brain subjected to normobaric hyperoxia as a model. This evidence concerns the gene DUSP1 and injury.