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Molecular hydrogen decelerates rheumatoid arthritis progression through inhibition of oxidative stress.

酸化ストレス抑制を介した分子状水素による関節リウマチ進行の遅延

animal study in vitro positive

Abstract

Using a collagen-induced arthritis (CIA) mouse model and rheumatoid arthritis fibroblast-like synoviocytes (RA-FLSs), this study investigated how molecular hydrogen affects inflammatory and oxidative processes. Hydrogen-enriched medium elevated superoxide dismutase (SOD) activity and reduced 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels following H₂O₂ exposure, indicating attenuation of oxidative DNA damage. H₂O₂-induced activation of MAPK, NF-κB, and TGF-β1 signaling was suppressed in hydrogen-treated cells. Additionally, molecular hydrogen was found to directly scavenge hydroxyl radicals and peroxynitrite, thereby reducing overall oxidative burden. These findings suggest that the protective effects of hydrogen on RA-FLSs are closely linked to inhibition of MAPK and NF-κB activation.

Mechanism

Molecular hydrogen directly scavenges hydroxyl radicals and peroxynitrite, and suppresses H₂O₂-induced activation of MAPK and NF-κB signaling as well as TGF-β1 expression in RA fibroblast-like synoviocytes, thereby reducing oxidative inflammation.

Bibliographic

Authors
Meng J, Yu P, Jiang H, Yuan T, Liu N, Tong J, et al.
Journal
Am J Transl Res
Year
2016
PMID
27830032
PMC
PMC5095341

Tags

Disease:関節炎・リウマチ Mechanism:抗酸化酵素 ヒドロキシルラジカル消去 炎症抑制 酸化ストレス ペルオキシナイトライト消去 活性酸素種

Delivery context

This is basic research at the cellular or molecular level. For human application, inhalation is the most promising delivery route, but inhalation carries explosion risk and concentration matters (empirical LFL of 10%; high-concentration devices are not recommended).

Safety notes

This is basic research at the cellular or molecular level. For human application, inhalation is the most promising delivery route, but inhalation carries explosion risk and concentration matters (empirical LFL of 10%; high-concentration devices are not recommended).

See also:

Other papers on the same disease / condition

Cite as: H2 Papers — PMID 27830032. https://h2-papers.org/en/papers/27830032
Source: PubMed PMID 27830032