新生仔ブタにおける窒息誘発性神経細胞COX-2発現に対する分子状水素の抑制効果
Using a neonatal piglet model of hypoxic-ischemic encephalopathy (HIE), this study examined whether asphyxia induces neuronal cyclooxygenase-2 (COX-2) and whether H2 inhalation modifies this response. Piglets underwent either 8 or 20 minutes of asphyxia, followed by inhalation of room air containing 2.1% H2 for 4 hours. Immunohistochemical analysis at 24 hours post-asphyxia revealed that severe HIE produced region-specific increases in COX-2-positive neurons within the parietal and occipital cortices and the CA3 hippocampal subfield. H2 inhalation substantially prevented these elevations. In the parietal cortex, reduced 8-hydroxy-2'-deoxyguanosine immunoreactivity and preserved microglial ramification index accompanied the attenuation of COX-2 induction, indicating concurrent reductions in oxidative stress and neuroinflammation. These findings establish that asphyxia elevates neuronal COX-2 in a region-dependent manner, and that H2 inhalation suppresses this pathway, potentially contributing to its neuroprotective properties.
H2 inhalation appears to suppress asphyxia-induced neuronal COX-2 upregulation by reducing oxidative stress (evidenced by decreased 8-OHdG immunoreactivity) and attenuating neuroinflammation (reflected by preserved microglial ramification), thereby limiting region-specific brain lesion progression in HIE.
For inhalation applications of molecular hydrogen, the lower flammability limit (LFL) deserves careful handling. The classical 4% figure applies to closed-system mixtures; the practical inhalation-environment threshold is 10%. Even pure-hydrogen output (the UFL 75% paradox) passes through the flammable range at the air–gas boundary. High-concentration (66% / 100%) inhalers are documented in the Japanese Consumer Affairs Agency accident-information database and are not recommended.
See also:
https://h2-papers.org/en/papers/29565041