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

Dan Xuan1, Dandan Feng1, Fuyong Qiang1

  • 1Department of Rheumatism and Immunology, The First Affiliated Hospital of Wannan Medical College, Wuhu,Anhui, 241000, China.

Allergologia Et Immunopathologia
|March 15, 2025
PubMed
Abstract

Insights

Dual oxidase 2 (DUOX1) suppresses rheumatoid arthritis (RA) progression by inhibiting inflammation and oxidative stress in synovial cells. Overexpression of DUOX1 reduces cell proliferation and migration via the NF-κB pathway.

Area of Science:

  • Biochemistry
  • Immunology
  • Cell Biology

Background:

  • Rheumatoid arthritis (RA) involves chronic inflammation in synovial cells.
  • Dual oxidase 2 (DUOX1) is implicated in cellular redox homeostasis.
  • The role of DUOX1 in RA pathogenesis requires further investigation.

Purpose of the Study:

  • To investigate the function of DUOX1 in fibroblast-like synoviocytes relevant to RA.
  • To elucidate the molecular mechanisms underlying DUOX1's action in RA.

Main Methods:

  • Utilized IL-1β-stimulated MH7A synovial fibroblasts.
  • Assessed cell viability, migration, inflammatory factors (ELISA), and reactive oxygen species (ROS) production.
  • Employed Western blotting to confirm DUOX1's antiarthritic mechanism and NF-κB pathway involvement.

Main Results:

  • IL-1β stimulation downregulated DUOX1, increasing cell proliferation, migration, inflammation, and oxidative stress.
  • DUOX1 overexpression inhibited IL-1β production, proliferation, migration, inflammation, and oxidative stress.
  • DUOX1 activation suppressed the nuclear factor kappa B (NF-κB) inflammatory pathway.

Conclusions:

  • DUOX1 acts as a suppressor of proliferation, migration, inflammation, and oxidative stress in RA synovial cells.
  • DUOX1 exerts its anti-inflammatory effects by inhibiting the NF-κB signaling pathway.
  • DUOX1 represents a potential therapeutic target for managing rheumatoid arthritis.
Keywords:
DUOX1NF-κBfibroblast-like synoviocytesinflammationoxidative stressrheumatoid arthritis

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