水素ガスは好中球細胞外トラップ（NET）の形成を抑制する
Neutrophil extracellular traps (NETs) are implicated in the pathogenesis of infectious and cardiovascular inflammatory conditions. This study examined whether H₂ exposure could suppress NET formation using neutrophils isolated from healthy human donors stimulated with PMA or the calcium ionophore A23187. H₂-exposed neutrophils showed reduced histone citrullination, chromatin-mediated membrane disruption, and NET component release compared with controls. H₂ also decreased Ser-139 phosphorylation of H2AX, a DNA damage marker, thereby lowering CXCR4 expression in NET-prone neutrophil subsets. Myeloperoxidase chlorination activity and reactive oxygen species production were suppressed to a degree comparable to N-acetylcysteine and ascorbic acid, yet H₂ demonstrated stronger NET inhibition than these antioxidants under PMA stimulation. For A23187-induced, ROS-independent NET formation, H₂ appeared to act through direct inhibition of peptidyl arginine deiminase 4 (PAD4)-mediated histone citrullination. In LPS-induced sepsis models (mice and aged mini pigs), H₂ inhalation reduced NET formation and component release in both blood and bronchoalveolar lavage fluid.
H₂ inhibits NET formation by scavenging reactive oxygen species, suppressing myeloperoxidase chlorination activity, directly inhibiting PAD4-mediated histone citrullination, and reducing H2AX Ser-139 phosphorylation to downregulate CXCR4 expression in neutrophils.
This study combines multiple delivery routes. As a general principle, the most efficient route for routine hydrogen intake is inhalation. Inhalation carries explosion risk (empirical LFL of 10%; high-concentration devices are documented in the Consumer Affairs Agency accident database and are not recommended).
See also:
https://h2-papers.org/en/papers/35257042