激しい急性運動による海馬炎症に対する吸入水素ガスの抑制効果：非運動習慣ラットを用いた検討
This study examined whether inhaled molecular hydrogen (2% H2) modulates hippocampal inflammation and oxidative stress in sedentary rats subjected to intense acute treadmill exercise. Animals ran in a sealed chamber while breathing either 2% H2 or a control gas mixture. Hippocampal tissue was collected immediately and 3 hours post-exercise. Exercise elevated TNF-α, IL-6, and IL-10 immediately after the session, with no change in IL-1β. H2 inhalation suppressed the exercise-induced rises in TNF-α and IL-6 while further amplifying the IL-10 response. Oxidative stress markers—SOD activity, TBARS, and NOx—were unaffected by either exercise or H2. All measured parameters returned to baseline levels by 3 hours post-exercise. These findings indicate that H2 exerts anti-inflammatory effects in the hippocampus by downregulating pro-inflammatory cytokines and upregulating anti-inflammatory cytokine production, without altering local oxidative stress status.
H2 inhalation reduces exercise-induced hippocampal inflammation by suppressing pro-inflammatory cytokines TNF-α and IL-6 while simultaneously enhancing the anti-inflammatory cytokine IL-10, without altering oxidative stress markers such as SOD, TBARS, or NOx.
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/31715290