水素ガスはNF-κB経路の抑制と炎症性サイトカイン産生低下を介してセボフルラン誘発神経毒性を軽減する：新生仔ラットを用いた検討
Neurotoxic effects of anesthetic agents on the developing brain represent a growing concern. Neonatal rats were exposed to sevoflurane alone or in combination with hydrogen gas for 2 hours, and cognitive performance was assessed at 10 weeks of age using Y-maze and fear-conditioning paradigms. Animals receiving sevoflurane alone showed impaired spatial recognition and fear memory relative to controls. Co-administration of hydrogen gas significantly restored cognitive function compared with sevoflurane exposure alone. At the molecular level, hydrogen gas inhibited NF-κB phosphorylation and its translocation into the nucleus, while also reducing the levels of interleukin-1β, interleukin-6, and tumor necrosis factor-α. These findings indicate that NF-κB pathway inhibition and attenuation of proinflammatory cytokine release are key mechanisms by which hydrogen gas counters sevoflurane-associated neurotoxicity in the neonatal rat brain.
Hydrogen gas inhibits NF-κB phosphorylation and nuclear translocation, thereby reducing the release of IL-1β, IL-6, and TNF-α, which collectively attenuates sevoflurane-induced neurotoxicity in the developing rat brain.
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/28926473