Molecular hydrogen alleviates asphyxia-induced neuronal cyclooxygenase-2 expression in newborn pigs

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 newborn pigs, and whether neuronal COX-2 levels were affected by H2 treatment. Piglets were subjected to either...

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Elmentve itt :
Bibliográfiai részletek
Szerzők: Varga Viktória Éva
Németh János
Oláh Orsolya
Tóth-Szűki Valéria
Kovács Viktória
Remzső Gábor
Domoki Ferenc
Dokumentumtípus: Cikk
Megjelent: 2018
Sorozat:ACTA PHARMACOLOGICA SINICA 39 No. 8
doi:10.1038/aps.2017.148

mtmt:3393020
Online Access:http://publicatio.bibl.u-szeged.hu/14829
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520 3 |a 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 newborn 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 neuroin fl ammation, 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-in fl ammatory neuroprotective effects of H2 treatment. 
700 0 1 |a Németh János  |e aut 
700 0 1 |a Oláh Orsolya  |e aut 
700 0 2 |a Tóth-Szűki Valéria  |e aut 
700 0 2 |a Kovács Viktória  |e aut 
700 0 2 |a Remzső Gábor  |e aut 
700 0 2 |a Domoki Ferenc  |e aut 
856 4 0 |u http://publicatio.bibl.u-szeged.hu/14829/1/Domoki_ActaPharmacolSin_2018.pdf  |z Dokumentum-elérés