虚血再灌流障害における分子状水素の保護的役割に関するレビュー
Ischemia-reperfusion injury (IRI) contributes substantially to morbidity and mortality across conditions such as acute coronary syndrome, cerebral stroke, and organ transplantation. Ischemia induces hypoxic cellular dysfunction, while the subsequent restoration of blood flow paradoxically amplifies damage through reactive oxygen species generation and inflammatory cascade activation. This review consolidates evidence on molecular hydrogen's protective effects against IRI across multiple organ systems—including the heart, brain, and transplanted organs—and examines the mechanistic basis of its action. As a selective antioxidant with anti-inflammatory, cytoprotective, and signal-modulatory properties, molecular hydrogen has demonstrated efficacy in diverse experimental models. Key mechanisms include suppression of oxidative stress and inflammatory signaling, enhancement of ATP synthesis, reduction of intracellular calcium overload, and modulation of cell death pathways. The authors conclude that further translational research is required before molecular hydrogen can be systematically incorporated into clinical protocols for IRI management.
Molecular hydrogen selectively scavenges reactive oxygen species, suppresses inflammatory signaling cascades, enhances mitochondrial ATP production, reduces intracellular calcium overload, and modulates apoptotic and other cell death pathways, collectively attenuating ischemia-reperfusion injury across organ systems.
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/39063126