DUOX1 inhibits the progression of rheumatoid arthritis by regulating the NF-κB pathway in vitro.

Abstract

Background: This study investigates the role of dual oxidase 2 (DUOX1) in fibroblast-like synoviocytes associated with rheumatoid arthritis (RA) and to elucidate its potential mechanism of action.

Method: The anti-inflammatory effects of DUOX1 were assessed using IL-1β (interleukin-1 beta)-stimulated synovial fibroblasts (MH7A). Cell viability and migration were evaluated using the Cell Counting Kit-8 and Transwell assays, respectively. Enzyme-linked immunosorbent assay (ELISA) was performed to measure cellular inflammatory factor levels, and immunofluorescence and specific kits were used to assess reactive oxygen species (ROS) production and redox indicators. Western blotting was performed to confirm the antiarthritic mechanism of DUOX1.

Result: The findings revealed that the stimulation if IL-1β downregulates DUOX1 expression in MH7A cells, leading to increased proliferation, migration, inflammatory responses, and oxidative stress. Conversely, DUOX1 overexpression increased the production of IL-1β inducing excessive proliferation, migration, inflammation, and oxidative stress in MH7A cells, and inhibited the activation of the nuclear factor kappa B (NF-κB) inflammatory pathway.

Conclusion: DUOX1 significantly suppresses the proliferation, migration, inflammation, and oxidative stress of RA synovial cells through the inhibition of the NF-κB signaling pathway.