水素水摂取によるNSAID誘発性腸症の改善：ROS低減と短鎖脂肪酸産生を介したメカニズムの検討
This mouse study examined how hydrogen-rich water (HRW) affects indomethacin-induced small intestinal injury. Oral HRW administration for 5 days significantly reduced histological damage and suppressed inflammatory cytokine expression. Luminal reactive oxygen species (ROS) were markedly decreased in HRW-treated animals. Although gut microbiota composition was not altered by HRW, fecal microbiota transplantation (FMT) from HRW-fed mice into recipient animals attenuated intestinal injury. Cecal short-chain fatty acid (SCFA) concentrations were significantly elevated in HRW-treated mice compared with controls. In vitro co-culture experiments showed that cecal supernatants from HRW-treated animals increased interleukin-10 expression in RAW264 macrophage cells. These findings indicate that HRW protects intestinal mucosa through two complementary mechanisms: direct ROS scavenging and SCFA-mediated anti-inflammatory signaling.
HRW exerts dual protective effects: direct scavenging of luminal ROS including hydroxyl radicals, and elevation of cecal short-chain fatty acids that promote IL-10 production in macrophages, thereby suppressing intestinal inflammation.
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/36478314