水素水がラットのLPS誘発性慢性腸炎に対してNrf-2およびNF-κBシグナル経路を介して示す保護効果
Chronic low-dose lipopolysaccharide (LPS) exposure disrupts intestinal barrier integrity and promotes both local and systemic inflammation. This animal study examined whether orally administered hydrogen-rich water could counteract LPS-induced chronic intestinal inflammation in rats. Animals received hydrogen-rich water for seven months before tail-vein injection of LPS at 200 μg/kg. Biochemical and histological analyses—including ELISA, Western blot, and immunohistochemistry—revealed that hydrogen-rich water elevated superoxide dismutase activity and tight-junction protein levels, activated the Nrf-2 signaling pathway, and suppressed pro-inflammatory mediators cyclooxygenase-2, myeloperoxidase, and reactive oxygen species. Concurrently, NF-κB pathway activation was markedly reduced. These findings indicate that hydrogen-rich water protects against LPS-driven chronic intestinal inflammation by modulating the interplay between Nrf-2 and NF-κB signaling cascades.
Hydrogen-rich water activates the Nrf-2 pathway to upregulate superoxide dismutase, while simultaneously suppressing NF-κB signaling, thereby reducing COX-2, myeloperoxidase, and ROS levels and preserving tight-junction protein integrity in the intestinal barrier.
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/36356098