水素水がマウス炎症性腸疾患モデルにおいて小胞体ストレス抑制とHO-1発現促進を介して腸管保護効果を示す
Using a dextran sulfate sodium (DSS)-induced murine model of inflammatory bowel disease (IBD), this study examined the intestinal protective effects of hydrogen-rich water (HRW) and the underlying mechanisms. Male mice were allocated to control, DSS, DSS+HRW, and DSS+HRW+ZnPP groups. HRW administration significantly reduced body weight loss, disease activity index, colon shortening, and colonic wall thickening compared with DSS-only animals. Oxidative stress markers MDA and MPO in colonic tissue were markedly lowered, while superoxide dismutase activity and glutathione levels increased. Pro-inflammatory cytokines TNF-α, IL-6, and IL-1β were substantially reduced. Key endoplasmic reticulum (ER) stress proteins—p-eIF2α, ATF4, XBP1s, and CHOP—were downregulated following HRW administration. HRW also upregulated heme oxygenase-1 (HO-1) expression, and co-administration of the HO-1 inhibitor ZnPP reversed these protective outcomes, implicating the HO-1 pathway as a critical mediator of HRW's effects.
HRW suppresses ER stress signaling proteins (p-eIF2α, ATF4, XBP1s, CHOP) and upregulates HO-1 expression, collectively reducing oxidative stress markers and pro-inflammatory cytokine levels to protect colonic tissue in DSS-induced IBD.
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/28293084