Molecular hydrogen decelerates rheumatoid arthritis progression through inhibition of oxidative stress

作者：Meng, Jia; Yu, Pan; Jiang, Hui; Yuan, Tao; Liu, Naicheng; Tong, Jian; Chen, Haiyan^*; Bao, Nirong^*; Zhao, Jianning^*

来源：American Journal of Translational Research, 2016, 8(10): 4472-4477.

• Rheumatoid arthritis
• hydrogen
• SOD
• NF-kappa B
• TGF-beta 1

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 H2O2 treatment and decrease 8-hydroxy-2'-deoxyguanosine (8-OHdG) level. Since H2O2 treatment activates MAPK, NF-kappa B and TGF-beta 1 in cells, our study suggested that H-2 could inhibit H2O2 activated MAPK and NF-kappa B activation as well as TGF-beta 1 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-kappa B pathway also play roles in oxidative damage caused by H2O2 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-kappa B.

• 出版日期2016
• 单位中国人民解放军第二军医大学; 南京大学