吸入水素ガスによる全身性炎症時の海馬神経炎症・グリア反応性の抑制と記憶障害の改善
Using a rat endotoxemia model induced by a single lipopolysaccharide (LPS) injection, this study examined how inhaled molecular hydrogen (H2) affects hippocampal neuroinflammation during systemic inflammation. Integrating approaches from hippocampal electrophysiology to behavioral testing, the investigators found that H2 inhalation reduced pro-inflammatory cytokine levels in both peripheral blood and hippocampal tissue. Microglial and astrocytic activation were also diminished. Behavioral assessments revealed attenuation of memory impairment, whereas long-term potentiation (LTP) remained unaffected. These findings represent the first reported evidence that inhaled H2 can suppress hippocampal microglial and astrocytic inflammatory responses, an effect associated with reduced cognitive deficits arising from systemic inflammation.
Inhaled H2 appears to reduce LPS-induced pro-inflammatory cytokine surges in the hippocampus by suppressing microglial and astrocytic activation, thereby limiting neuroinflammation and associated memory deficits without altering long-term potentiation.
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/37449286