水素水摂取による腸内細菌叢・短鎖脂肪酸経路を介した動脈硬化抑制効果
Using ApoE-knockout mice as an atherosclerosis model, this study examined how hydrogen-rich water (HW) consumption affects plaque development and vascular stability. HW-fed animals showed marked reductions in plaque burden alongside altered gut microbial community structure and modified short-chain fatty acid (SCFA) profiles. Antibiotic-mediated microbiota depletion eliminated the protective phenotype, whereas fecal microbiota transplantation from HW-treated donors reproduced anti-atherosclerotic effects in recipient mice, confirming a gut microbiota-dependent mechanism. Propionate concentrations rose significantly in both cecal contents and serum of HW-treated animals. In vitro experiments demonstrated that propionate directly inhibited M1 macrophage polarization and attenuated inflammatory signaling. Collectively, the findings identify a gut microbiota–propionate–macrophage axis as a central pathway through which HW reduces vascular inflammation and plaque progression.
HW reshapes gut microbial composition, elevating propionate levels in cecal contents and serum; propionate in turn suppresses M1 macrophage polarization and inflammatory signaling, thereby reducing atherosclerotic plaque formation and improving plaque stability.
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).
See also:
https://h2-papers.org/en/papers/42069299