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Cyclooxygenase-2 (COX-2) has an established role in the pathogenesis of hypoxic-ischemic encephalopathy (HIE).In this study we sought to determine whether COX-2 was induced by asphyxia in newb pigs,and whether neuronal COX-2 levels were affected by H2 treatment.Piglets were subjected to either 8 min of asphyxia or a more severe 20 min of asphyxia followed by H2 treatment (inhaling room air containing 2.1％ H2 for 4 h).COX-2 immunohistochemistry was performed on brain samples from surviving piglets 24 h after asphyxia.The percentages of COX-2-immunopositive neurons were determined in cortical and subcortical areas.Only in piglets with more severe HIE,we observed significant,region-specific increases in neuronal COX-2 expression within the parietal and occipital cortices and in the CA3 hippocampal subfield.H2 treatment essentially prevented the increases in COX-2-immunopositive neurons.In the parietal cortex,the attenuation of COX-2 induction was associated with reduced 8’-hydroxy-2’-deoxyguanozine immunoreactivity and retained microglial ramifcation index,which are markers of oxidative stress and neuroinflammation,respectively.This study demonstrates for the first time that asphyxia elevates neuronal COX-2 expression in a piglet HIE model.Neuronal COX-2 induction may play region-specific roles in brain lesion progression during HIE development,and inhibition of this response may contribute to the antioxidant/anti-inflammatory neuroprotective effects of H2 treatment.