高齢マウスのLPS誘発炎症モデルにおける2%水素ガス持続吸入による肺障害軽減効果
Against the backdrop of rising sepsis incidence in aging populations, this animal study examined the effects of hydrogen gas inhalation on LPS-induced systemic inflammation in 21–23-month-old male mice. Eight experimental groups were established, varying H2 concentration (1% or 2%) and exposure duration (1, 6, or 24 hours). Only the 24-hour 2% H2 inhalation regimen produced significant improvements: survival rates and locomotor activity increased, while mRNA levels of inflammatory markers in lung and liver tissue declined. Lung-specific senescence-associated molecules—including CXCL2, MMP-3, arginase-1, and the cell-cycle inhibitor p21—were also downregulated. Hepatic injury induced by LPS was not meaningfully altered under any tested condition. These findings indicate that prolonged, higher-concentration H2 inhalation selectively modulates pulmonary inflammation and aging-related molecular signatures in elderly mice.
Continuous inhalation of 2% H2 for 24 hours suppressed mRNA expression of inflammatory cytokines and senescence-associated proteins (CXCL2, MMP-3, arginase-1, p21) in lung tissue, thereby reducing LPS-induced pulmonary injury in aged 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/37572992