糖尿病ラットの脳卒中後における分子状水素の神経回復効果：TLR4/NF-κB炎症経路を介したメカニズム
Diabetes mellitus amplifies inflammatory responses and constitutes an independent risk factor for stroke, worsening neurological outcomes. Using a middle cerebral artery occlusion (MCAO) model in diabetic rats, this study evaluated the effects of molecular hydrogen (H2) across multiple endpoints: blood glucose levels before and after MCAO, 48-hour cerebral edema and infarct volume, and 28-day body weight, survival rate, and neurological function. Levels of TLR4, NF-κB p65 phosphorylation, catecholamines, acetylcholine, and inflammatory mediators were also quantified. H2 administration improved survival, body weight, and long-term neurological function while significantly reducing inflammation through suppression of NF-κB phosphorylation. Blood glucose fluctuations associated with MCAO were also attenuated. Notably, the beneficial effects were independent of circadian rhythm, suggesting favorable translational properties. These findings indicate that H2 exerts neurorestoration in diabetic stroke conditions through modulation of the TLR4/NF-κB signaling axis.
H2 suppresses phosphorylation of NF-κB p65 within the TLR4/NF-κB signaling pathway, thereby reducing downstream inflammatory mediator production and promoting neurological recovery in diabetic stroke.
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/35895245