分子状水素は敗血症誘発性心筋症においてゴルジストレス介在性のオートファジー・炎症・アポトーシスを調節することで心保護効果を発揮する
Sepsis-induced cardiomyopathy (SIC) represents a leading contributor to sepsis mortality. Using a caecal ligation and puncture (CLP) mouse model, this study examined the effects of 2% H2 inhalation on cardiac outcomes. CLP reduced 7-day survival, impaired cardiac function, elevated myocardial damage enzymes, and was accompanied by Golgi apparatus (GA) structural changes alongside heightened autophagy, inflammation, and apoptosis. Inhalation of 2% H2 reversed these deteriorations. Critically, co-administration of the GA stress-specific agonist Brefeldin A abolished the beneficial effects of H2, confirming that Golgi stress is a key mediator. Immunofluorescence and electron microscopy corroborated GA morphological alterations. These findings indicate that H2 confers cardiac protection in SIC by suppressing Golgi stress and its downstream cascades governing autophagy, inflammatory signaling, and cell death pathways.
H2 inhalation suppresses Golgi apparatus stress in septic cardiomyocytes, thereby reducing downstream activation of autophagy, pro-inflammatory signaling, and apoptotic pathways, collectively attenuating myocardial injury in CLP-induced sepsis.
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/40717465