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

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, H(2) enriched medium can increase super oxide dismutase (SOD) level following H(2)O(2) treatment and decrease 8-hydroxy-2’-deoxyguanosine (8-OHdG) level. Since H(2)O(2) treatment activates MAPK, NF-κB and TGF-β1 in cells, our study suggested that H(2) could inhibit H(2)O(2) activated MAPK and NF-κB activation as well as TGF-β1 expression in treated cells. Taken together, our data suggested that H(2) can directly neutralize OH and ONOO(-) to reduce oxidative stress. Moreover, MAPK and NF-κB pathway also play roles in oxidative damage caused by H(2)O(2) in RA-FLSs. H(2) can provide protection to cells against inflammation, which may be related to inhibition of the activation of MAPK and NF-κB.