定量プロテオミクスによる高酸素誘発性傷害に対する水素の保護機序の解明：II型肺胞上皮細胞を用いた検討
To clarify the molecular basis of hydrogen-mediated protection against hyperoxia-induced lung injury, primary type II alveolar epithelial cells (AECIIs) were cultured under three conditions for 24 hours: normoxia (21% O2), hyperoxia (95% O2), and hyperoxia combined with hydrogen. TMT-labeling quantitative proteomics was applied to profile protein expression changes. Hydrogen exposure under hyperoxic conditions improved cell viability, reduced apoptosis (reflected by altered Bax/Bcl-2 ratios), restored cell morphology, and promoted transdifferentiation toward type I alveolar epithelial cells. Among 5,782 proteins identified, 162 showed significant abundance changes under hyperoxia, while 97 were significantly altered by hydrogen co-treatment. Gene Ontology and KEGG pathway enrichment analyses implicated VEGFA, PDGFB, IGFBP3, EDN1, NADPH oxidase, and the coagulation cascade as key components of the protective response, indicating that hydrogen engages multiple biological processes to counteract hyperoxic damage in AECIIs.
Hydrogen modulates multiple proteins and pathways—including VEGFA, PDGFB, IGFBP3, EDN1, NADPH oxidase, and the coagulation cascade—to suppress apoptosis and improve viability in type II alveolar epithelial cells exposed to hyperoxia.
This is basic research at the cellular or molecular level. For human application, inhalation is the most promising delivery route, but inhalation carries explosion risk and concentration matters (empirical LFL of 10%; high-concentration devices are not recommended).
See also:
https://h2-papers.org/en/papers/30973277