腸内細菌叢を介した水素ガス吸入による大腸炎軽減：TLR4/NF-κBおよびNrf2経路の関与
Using a dextran sulfate sodium (DSS)-induced murine colitis model, this study examined how H₂ gas inhalation affects gut microbial composition and downstream inflammatory pathways. H₂ inhalation corrected DSS-induced dysbiosis by reducing potentially pathogenic taxa such as Enterobacteriaceae and Escherichia-Shigella while enriching beneficial genera including Bacteroides and Lactobacillaceae. Intestinal barrier integrity was restored through increased goblet cell density and upregulation of tight junction proteins ZO-1 and occludin. Immune balance was improved via normalization of the Treg/Th17 cell ratio. At the molecular level, suppression of TLR4/NF-κB signaling and activation of the Keap1/Nrf2 antioxidant axis were observed, accompanied by decreased pro-inflammatory cytokines, reduced oxidative stress markers, and elevated antioxidant enzyme activity. Fecal microbiota transplantation experiments corroborated these findings, supporting gut microbiome remodeling as a central mechanism underlying H₂-associated colitis alleviation.
H₂ inhalation reshapes gut microbial ecology, suppresses TLR4/NF-κB inflammatory signaling, and activates the Keap1/Nrf2 antioxidant pathway, collectively reducing cytokine production, oxidative stress, and intestinal barrier disruption in DSS-induced colitis.
For inhalation applications of molecular hydrogen, the lower flammability limit (LFL) deserves careful handling. The classical 4% figure applies to closed-system mixtures; the practical inhalation-environment threshold is 10%. Even pure-hydrogen output (the UFL 75% paradox) passes through the flammable range at the air–gas boundary. High-concentration (66% / 100%) inhalers are documented in the Japanese Consumer Affairs Agency accident-information database and are not recommended.
See also:
https://h2-papers.org/en/papers/41076929