水素水投与が新生仔ラットの気管支肺異形成症（BPD）に及ぼす改善効果
Bronchopulmonary dysplasia (BPD) involves arrested alveolar development and is closely linked to oxidative stress. A rat BPD model was established by injecting lipopolysaccharide (LPS) into amniotic fluid at embryonic day 16.5, while mothers consumed hydrogen-rich water from day 9.5 through the nursing period. Hydrogen-rich water normalized LPS-induced alveolar enlargement at postnatal days 7 and 14, and reduced pulmonary nitrotyrosine and 8-OHdG staining. LPS-suppressed expression of FGFR4, VEGFR2, and HO-1 genes was restored by hydrogen, whereas SOD1 expression was unaffected by either treatment. Inflammatory proteins TNF-α and IL-6, elevated by LPS, were reduced with hydrogen. In A549 human lung epithelial cells, 24-hour exposure to 10% hydrogen gas lowered reactive oxygen species production in both LPS-treated and control conditions. The absence of known adverse effects positions hydrogen as a candidate intervention for BPD.
Hydrogen reduces pulmonary reactive oxygen species, nitrotyrosine, and 8-OHdG, restores expression of FGFR4, VEGFR2, and HO-1, and suppresses TNF-α and IL-6 inflammatory signaling, collectively supporting normal alveolar development.
This study combines multiple delivery routes. As a general principle, the most efficient route for routine hydrogen intake is inhalation. Inhalation carries explosion risk (empirical LFL of 10%; high-concentration devices are documented in the Consumer Affairs Agency accident database and are not recommended).
See also:
https://h2-papers.org/en/papers/26845501