水素ガスによるCaco-2細胞の虚血再灌流障害後ミトコンドリア膜電位および呼吸機能の回復促進
Using Caco-2 intestinal epithelial cells as an in vitro ischemia-reperfusion (I/R) model, this study examined how hydrogen-rich gas (99% H2, 1% O2) affects mitochondrial function after hypoxic exposure of 3, 6, or 24 hours followed by reoxygenation. Compared with nitrogen-based hypoxia controls, hydrogen-treated cells showed marked improvements in mitochondrial membrane potential, oxygen consumption rate, and ATP production during the reperfusion phase. Reactive oxygen species levels were reduced, and pro-apoptotic signaling was suppressed. Notably, expression of HIF1α and PDK1 was downregulated in hydrogen-exposed cells, indicating that molecular hydrogen may act upstream of hypoxia-driven metabolic reprogramming. These findings suggest that hydrogen supports oxidative phosphorylation and overall cellular energy metabolism under I/R conditions, providing mechanistic insight relevant to intestinal and other hypoxia-related pathologies.
Molecular hydrogen downregulates HIF1α and PDK1 expression, thereby modulating hypoxia-driven signaling upstream. This promotes oxidative phosphorylation, restores mitochondrial membrane potential and ATP production, improves oxygen consumption, and reduces reactive oxygen species in I/R-injured intestinal cells.
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/41043278