水素吸入がオートファジー促進を介してマウスの敗血症性心筋症を軽減する
Sepsis-induced cardiomyopathy (SIC) affects 40–60% of septic patients and substantially elevates mortality risk. Using a cecal ligation and puncture (CLP) mouse model, this study investigated whether 2% H2 inhalation confers cardiac protection and explored the underlying autophagic mechanism. C57BL/6J male mice were allocated to sham, sham+H2, CLP, and CLP+H2 groups. H2-treated septic mice showed significantly improved 7-day survival, reduced myocardial inflammation, lower serum cardiac troponin I (cTnI) levels, enhanced autophagy flux, and altered mitophagy-related protein expression. To confirm the autophagic pathway, the autophagy inhibitor bafilomycin A1 (BafA1, 1 mg/kg intraperitoneally) was administered post-CLP. BafA1 co-treatment reversed the H2-associated improvements in survival, myocardial injury scores, and cTnI levels, indicating that autophagy flux is essential for the cardioprotective action of H2 in sepsis.
H2 inhalation promotes autophagy flux and mitophagy in cardiac tissue, thereby reducing myocardial inflammation and injury in septic mice. Blockade of autophagy with bafilomycin A1 abolished these protective effects, confirming the autophagic pathway as the key mediator.
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/38395800