敗血症関連脳症マウスモデルにおける水素ガス吸入の認知機能保護効果
This animal study examined whether inhaled hydrogen gas (2% H2) could protect cognitive function in male ICR mice subjected to cecal ligation and puncture (CLP)-induced sepsis-associated encephalopathy (SAE). Eighty-four mice were allocated to four groups: sham, sham+H2, sepsis, and sepsis+H2. Hydrogen was administered for 1 hour at 1 and 6 hours post-operation. At 24 hours, CLP mice showed marked neuronal damage in hippocampal CA1, reduced superoxide dismutase (SOD) and catalase (CAT) activities, and elevated malondialdehyde (MDA) and 8-iso-prostaglandin F2α levels in serum and hippocampus. H2 inhalation significantly reversed these changes. Behavioral assessments via Y-maze and fear-conditioning tests conducted from days 3 to 14 revealed that H2-treated septic mice spent more time in novel zones and exhibited higher freezing percentages compared with untreated septic controls. The findings suggest that enhanced antioxidant enzyme activity and reduced oxidative stress markers underlie the neuroprotective effects observed.
H2 inhalation elevated superoxide dismutase and catalase activities while reducing lipid peroxidation markers (MDA and 8-iso-PGF2α) in serum and hippocampus, thereby attenuating neuronal damage in the CA1 region and preserving cognitive function in CLP-induced septic mice.
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/25573317