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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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Emodin Attenuates Rheumatoid Arthritis by Modulating the NF-κB/HIF-1α/VEGF Signaling Pathway.

Dehao Du1, Yihang Lou2, Linlan Zhou1

  • 1Department of Combination of Chinese and Western Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.

International Journal of Molecular Sciences
|May 4, 2026
PubMed
Summary
This summary is machine-generated.

Emodin (EMO) effectively treats rheumatoid arthritis (RA) by inhibiting the NF-κB/HIF-1α/VEGF pathway, reducing inflammation and pathological angiogenesis. This natural compound shows promise as a novel therapeutic agent for RA.

Keywords:
NF-κBemodinhypoxiapannusrheumatoid arthritis

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Area of Science:

  • Rheumatology
  • Pharmacology
  • Molecular Biology

Background:

  • Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by joint inflammation and destruction.
  • Pathological angiogenesis, driven by the NF-κB/HIF-1α/VEGF axis, plays a crucial role in RA pathogenesis.
  • Current treatments for RA have limitations, necessitating the exploration of novel therapeutic agents.

Purpose of the Study:

  • To evaluate the therapeutic efficacy of emodin (EMO) in rheumatoid arthritis (RA).
  • To investigate the underlying mechanism of EMO's action, focusing on the NF-κB/HIF-1α/VEGF signaling pathway.
  • To assess EMO's impact on pathological angiogenesis and inflammatory responses in RA models.

Main Methods:

  • Bovine type II collagen-induced arthritis (CIA) mouse models and LPS-stimulated EA.hy926 endothelial cells were used.
  • Histopathological analysis, Western blotting, IHC, immunofluorescence, and tube formation assays assessed EMO's effects.
  • siRNA interference was employed to validate molecular mechanisms.

Main Results:

  • EMO treatment significantly attenuated joint inflammation, synovial hyperplasia, and bone destruction in CIA mice.
  • EMO downregulated key proteins in the NF-κB/HIF-1α/VEGF axis and reduced pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) in vitro.
  • siRNA knockdown of p65 confirmed the EMO-mediated inhibition of angiogenesis via this pathway.

Conclusions:

  • EMO demonstrates significant therapeutic efficacy in preclinical models of rheumatoid arthritis.
  • EMO alleviates RA pathology by inhibiting the NF-κB signaling pathway, thereby suppressing pathological angiogenesis and inflammation.
  • EMO holds potential as a novel therapeutic agent for rheumatoid arthritis.