卵白アルブミン誘発喘息マウスモデルにおける水素ガス吸入による気道炎症および酸化ストレスの軽減
Allergic asthma, characterized by chronic airway inflammation, poses a significant global health burden. This animal study investigated the effects of 3% hydrogen gas inhalation in a BALB/c mouse model of ovalbumin (OVA)-induced allergic asthma. Thirty female mice were allocated to five groups: non-treatment, hydrogen-only, OVA-only negative control, OVA plus intranasal salbutamol positive control, and OVA plus inhaled hydrogen. Endpoints included differential white blood cell counts, lung histology, pro-inflammatory cytokines (IL-4, IL-5, IL-13, TNF-α, IFN-γ, GM-CSF, IL-10), oxidative stress markers (ROS, NO), antioxidant enzymes (GPx, catalase), and serum IgE. Hydrogen inhalation significantly reduced inflammatory cell infiltration, suppressed pro-inflammatory cytokine levels, enhanced antioxidant enzyme activity, and lowered serum IgE concentrations compared with the OVA-only control group.
Inhaled H2 scavenges reactive oxygen species and nitric oxide while upregulating glutathione peroxidase and catalase activity, thereby suppressing pro-inflammatory cytokines (IL-4, IL-5, IL-13, TNF-α) and reducing IgE-mediated allergic airway inflammation.
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/39594470