ラクツロース経口投与による腸内水素産生増加がDSS誘発大腸炎を抑制するメカニズムの検討
A mouse model of ulcerative colitis was established using dextran sodium sulfate (DSS), and the effects of oral lactulose at three doses (0.1, 0.15, and 0.2 ml/10 g) were compared with intraperitoneal hydrogen-rich saline over 7 days. Lactulose administration significantly reduced DSS-induced body weight loss, elevated colitis scores, colon shortening, and histopathological damage. Colonic levels of TNF-α, IL-1β, malondialdehyde (MDA), and myeloperoxidase (MPO) were also markedly decreased. Co-administration of oral antibiotics substantially diminished these protective effects and concurrently reduced exhaled H2 concentrations as measured by breath testing. The findings indicate that colonic microflora ferment lactulose to generate endogenous H2, which in turn attenuates oxidative stress and inflammatory responses in DSS-injured colon tissue.
Colonic microflora ferment orally ingested lactulose to produce H2, which scavenges reactive oxygen species and suppresses pro-inflammatory mediators including TNF-α, IL-1β, MDA, and MPO in DSS-damaged colon tissue.
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/23371012