水素による代謝経路スイッチの逆転を介したアレルギー性気道炎症の抑制機序
This observational and experimental study investigated whether molecular hydrogen exerts anti-inflammatory effects through modulation of energy metabolic reprogramming. In monocytes from asthmatic patients and in lungs of ovalbumin-sensitized mice, elevated lactate production and glycolytic enzyme activities were accompanied by reduced ATP output and diminished mitochondrial respiratory chain complex I and III activities, indicating a shift from oxidative phosphorylation to aerobic glycolysis. Hydrogen administration to sensitized mice reversed this metabolic switch, suppressed upregulation of glycolytic enzymes and hypoxia-inducible factor-1α, and restored expression of mitochondrial respiratory chain complexes and PGC-1α. Additionally, hydrogen counteracted the downregulation of sirtuins 1, 3, 5, and 6. These findings suggest that hydrogen modulates energy metabolic reprogramming at multiple regulatory levels, thereby reducing allergic airway inflammation.
Hydrogen suppresses HIF-1α and glycolytic enzyme upregulation while restoring PGC-1α and sirtuins 1, 3, 5, and 6 expression, thereby reversing the metabolic shift from aerobic glycolysis back to mitochondrial oxidative phosphorylation and reducing airway inflammation.
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/32029879