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10.1038/aps.2017.148 http://scihub22266oqcxt.onion/10.1038/aps.2017.148 29565041/?report=reader!6289359!29565041     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Acta+Pharmacol+Sin 2018 ; 39 (8): 1273-1283 Nephropedia Template TP {{tp|p=29565041|t=2018. Molecular hydrogen alleviates asphyxia-induced neuronal cyclooxygenase-2 expression in newborn pigs |pdf=|usr=}}{{29565041}} gab.com Text Molecular hydrogen alleviates asphyxia-induced neuronal cyclooxygenase-2 expression in newborn pigs JO: Acta Pharmacol Sin http://www.kidney.de/pget.php?&tw=1&pmid=29565041 #FOAvip 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 H(2) treatment. Piglets were subjected to either 8 min of asphyxia or a more severe 20 min of asphyxia followed by H(2) treatment (inhaling room air containing 2.1% H(2) 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. H(2) 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 neuroinfiammation, 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-infiammatory neuroprotective effects of H(2) treatment. Twit Text FOAVip Molecular hydrogen alleviates asphyxia-induced neuronal cyclooxygenase-2 expression in newborn pigs ????Acta Pharmacol Sin http://www.kidney.de/pget.php?&tw=1&pmid=29565041 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29565041 #FOAvip English Wikipedia <ref>{{Cite pmid|29565041}}</ref> Molecular hydrogen alleviates asphyxia-induced neuronal cyclooxygenase-2 expression in newborn pigs #MMPMID29565041 Varga V; Nemeth J; Olah O; Toth-Szuki V; Kovacs V; Remzso G; Domoki F Acta Pharmacol Sin 2018[Aug]; 39 (8): 1273-1283 PMID29565041show ga 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 H(2) treatment. Piglets were subjected to either 8 min of asphyxia or a more severe 20 min of asphyxia followed by H(2) treatment (inhaling room air containing 2.1% H(2) 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. H(2) 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 neuroinfiammation, 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-infiammatory neuroprotective effects of H(2) treatment. |Animals[MESH] |Animals, Newborn[MESH] |Asphyxia/*prevention & control[MESH] |Cyclooxygenase 2/*metabolism[MESH] |Hippocampus/physiopathology[MESH] |Hydrogen/*therapeutic use[MESH] |Hypoxia-Ischemia, Brain/*prevention & control[MESH] |Male[MESH] |Microglia/metabolism[MESH] |Neurons/metabolism[MESH] |Neuroprotective Agents/*therapeutic use[MESH] |Parietal Lobe/physiopathology[MESH]Molecular hydrogen alleviates asphyxia-induced neuronal cyclooxygenase(epmc).pdf DeepDyve Pubget Overpricing