Molecular hydrogen demonstrates significant therapeutic potential in decelerating rheumatoid arthritis progression by directly neutralizing reactive oxygen species (OH and ONOO-) and inhibiting key inflammatory signaling pathways (MAPK and NF-κB) in fibroblast-like synovial cells. These findings suggest that hydrogen therapy may provide a novel protective mechanism against oxidative stress-induced inflammation and joint destruction in rheumatoid arthritis, warranting further clinical investigation.
Plain-Language Summary
Researchers tested whether molecular hydrogen could reduce inflammation in mice with a type of arthritis similar to rheumatoid arthritis. They found that hydrogen-enriched water appeared to protect cells from damage caused by oxidative stress (harmful molecules that build up in the body) by activating protective enzymes and blocking inflammatory signaling pathways that normally trigger joint damage.
Abstract
Rheumatoid arthritis (RA) is a chronic inflammatory disease which results in progressive destruction of the joint. In this study, we examined if the hydrogen could inhibit inflammation in a mouse model of collagen-induced arthritis (CIA) via oxidative stress on RA-FLSs. Moreover, to identify the mechanisms of action, we evaluated the effect of hydrogen on RA-FLSs development and the expression of pro-inflammatory cytokines and signaling pathways. Based on our result, H2 enriched medium can increase super oxide dismutase (SOD) level following H2O2 treatment and decrease 8-hydroxy-2'-deoxyguanosine (8-OHdG) level. Since H2O2 treatment activates MAPK, NF-κB and TGF-β1 in cells, our study suggested that H2 could inhibit H2O2 activated MAPK and NF-κB activation as well as TGF-β1 expression in treated cells. Taken together, our data suggested that H2 can directly neutralize OH and ONOO- to reduce oxidative stress. Moreover, MAPK and NF-κB pathway also play roles in oxidative damage caused by H2O2 in RA-FLSs. H2 can provide protection to cells against inflammation, which may be related to inhibition of the activation of MAPK and NF-κB.
