水素分子による抗デスモグレイン1抗体誘発性天疱瘡関連間質性肺疾患への効果:酸化ストレス抑制を介したメカニズムの検討
Pemphigus-associated interstitial lung disease (P-ILD) involves pulmonary interstitial inflammation and fibrosis as a serious complication of pemphigus. Using BALB/cJGpt mice, this study found that anti-desmoglein (Dsg) 1 antibodies, but not anti-Dsg3 antibodies, were responsible for inducing interstitial inflammation and fibrosis. Immunofluorescence analysis revealed IgG deposition in the alveolar epithelium, indicating immune complex formation and epithelial damage. Gene expression profiling showed elevated pro-inflammatory cytokines and upregulated fibrotic markers, alongside impaired reactive oxygen species metabolism. Administration of hydrogen-rich water to P-ILD mice significantly reduced oxidative stress, suppressed interstitial inflammation, and prevented pulmonary fibrosis progression. These findings indicate that anti-Dsg1 antibodies and oxidative damage are central to P-ILD pathogenesis, and that molecular hydrogen's antioxidant capacity can restore redox balance and protect against lung injury in this model.
Molecular hydrogen restores the pro-oxidant–antioxidant balance by scavenging reactive oxygen species, thereby reducing oxidative damage that drives anti-Dsg1 antibody-induced pulmonary interstitial inflammation and fibrosis progression.
Hydrogen-rich water is a low-risk delivery route, but the achievable systemic hydrogen dose is bounded. For clinical applications, inhalation is the most efficient route; inhalation, however, carries explosion risk, and concentration matters (empirical LFL of 10% applies to inhalation environments; high-concentration devices are documented in the Consumer Affairs Agency accident database and are not recommended).
See also:
https://h2-papers.org/en/papers/40362440