水素水の抗酸化・抗炎症作用によるエタノール誘発性脂肪肝の軽減：マウスを用いた検討
This mouse study examined the hepatoprotective potential of hydrogen-rich water (HRW) against chronic ethanol (EtOH)-induced fatty liver. Female mice received a Lieber-DeCarli liquid diet with EtOH for 12 weeks; HRW was administered orally at 1.2 mL per mouse three times daily. Silymarin served as a positive comparator. HRW directly scavenged hydrogen peroxide in a chemiluminescence assay. Serum alanine aminotransferase, aspartate aminotransferase, triglycerides, and total cholesterol were all significantly reduced by HRW. Hepatic lipid accumulation decreased, and pro-inflammatory cytokines TNF-α and IL-6 were suppressed, while anti-inflammatory IL-10 and IL-22 levels rose. Oxidative stress markers improved: malondialdehyde declined, glutathione was restored, and superoxide dismutase, glutathione peroxidase, and catalase activities increased. Acyl ghrelin expression was also elevated, potentially mediating cytokine modulation.
HRW elevates acyl ghrelin expression, which suppresses pro-inflammatory cytokines TNF-α and IL-6 while inducing IL-10 and IL-22. Concurrently, antioxidant enzymes including superoxide dismutase, glutathione peroxidase, and catalase are activated, reducing hepatic oxidative stress and lipid peroxidation.
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).
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https://h2-papers.org/en/papers/28785146