水素による肺動脈性肺高血圧症の改善：ラットモデルにおける抗炎症・抗酸化メカニズムの検討
Pulmonary arterial hypertension (PAH) involves reactive oxygen species and inflammatory processes in its pathogenesis. This study examined the effects of hydrogen-saturated water in a monocrotaline (MCT)-induced PAH rat model. Male Sprague-Dawley rats were divided into three groups: MCT plus hydrogen-saturated water, MCT plus dehydrogenized water, and saline plus dehydrogenized water. Hemodynamic assessment and morphometric pulmonary vascular analysis were performed 16 days after substance administration. Compared with the MCT-only group, hydrogen-treated animals showed significantly reduced pulmonary arterial pressure, preserved vascular density, decreased adventitial macrophage accumulation, lower 8-hydroxy-deoxyguanosine-positive cell counts, and reduced expression of stromal cell-derived factor-1 and monocyte chemoattractant protein-1. Phosphorylated STAT3 and NFAT expression levels were also markedly lower in the hydrogen group. These findings indicate that hydrogen-rich water intake attenuates MCT-induced PAH through suppression of oxidative stress, macrophage infiltration, and modulation of the STAT3/NFAT signaling axis.
Hydrogen-rich water intake suppressed macrophage accumulation in the pulmonary adventitia, reduced oxidative DNA damage (8-OHdG), and downregulated phosphorylated STAT3 and NFAT expression, collectively attenuating MCT-induced pulmonary arterial hypertension.
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).
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https://h2-papers.org/en/papers/26095621