分子状水素はNLRP3インフラマソーム抑制を介して外傷性脳損傷誘発性肺傷害を軽減する
Using a controlled cortical impact mouse model of traumatic brain injury (TBI), this study examined the effects of 2% hydrogen gas inhalation administered for 60 minutes beginning at 1 and 6 hours post-injury. TBI activated pulmonary NLRP3 inflammasome signaling, elevating ASC and caspase-1 expression and increasing secretion of IL-1β and IL-18. Hydrogen inhalation significantly reduced histopathological lung damage, apoptosis (TUNEL assay), wet-to-dry weight ratio, myeloperoxidase activity, and bronchoalveolar lavage fluid protein content. Co-administration of hydrogen with the selective NLRP3 inhibitor MCC950 (10 mg/kg intraperitoneally, 30 minutes before TBI) conferred greater pulmonary protection than either intervention alone, indicating that NLRP3 inflammasome inhibition is a central mechanism underlying hydrogen-mediated attenuation of TBI-induced lung injury.
Inhaled 2% hydrogen suppresses NLRP3 inflammasome activation in lung tissue, reducing caspase-1 cleavage and downstream secretion of IL-1β and IL-18, thereby attenuating TBI-induced pulmonary inflammation and apoptosis.
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/40405232