水素吸入による早期M2マクロファージ極性化誘導を介した皮膚創傷治癒における炎症抑制
Macrophages are central regulators of wound healing, particularly during the inflammatory phase. Using a dorsal full-thickness skin defect mouse model, this study examined the temporal effects of H2 inhalation on macrophage polarization. H2 inhalation promoted M1-to-M2 polarization approximately 2–3 days earlier than observed in standard wound healing (occurring on post-wounding days 2–3), while preserving M1 macrophage functionality. Time-series analyses integrating transcriptomics, peripheral blood cell counts, and cytokine profiling indicated that circulating monocytes serve as a primary source of H2-induced M2 macrophages. Furthermore, the polarization-promoting effects of H2 appeared to extend beyond its known antioxidant properties, suggesting additional mechanistic pathways. These findings indicate that H2 inhalation may reduce wound-associated inflammation by accelerating early macrophage phenotype switching.
H2 inhalation accelerates M1-to-M2 macrophage polarization within 2–3 days post-wounding, with peripheral blood monocytes as the cellular source. The mechanism involves pathways beyond antioxidant activity, reducing inflammatory signaling during the early wound healing phase.
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/37375833