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September 10, 2025Open Access

Inhibition of Nuclear factor kappa B ameliorates bone destruction and osteoclastogenesis in collagen-induced arthritis mice

Key Points

Inhibition of NF-κB alleviated bone destruction and reduced inflammation in collagen-induced arthritis mouse models.
Paw edema and arthritis scores were significantly lower in NF-κB inhibitor groups than in collagen-induced arthritis groups at various time points.
Key inflammatory markers such as IL-1β, MMP-1, and TNF-α showed decreased mRNA levels following NF-κB inhibition treatment.
This research indicates potential therapeutic avenues for treating inflammatory bone diseases linked to osteoclastogenesis.

Abstract

Background: We aimed to investigate the effect of interleukin-1β (IL-1β)/nuclear factor κB (NF-κB) pathway on osteoclastogenesis and inflammatory bone destruction in a mouse model of collagen-induced arthritis (CIA).Methodology: DBA/1 mice were divided into CIA group, NF-κB inhibitor group and control group. The degree of paw edema was measured and the score of paw arthritis was assessed. mRNA levels of IL-1β, matrix metalloproteinase-1 (MMP-1), tumour necrosis factor-α (TNF-α) levels, anti-tartrate acid phosphatase (TRAP), matrix metalloproteinase-9 (MMP-9), tissue proteinase K (CtsK) and integrin β3 (β3-Integrin) in the joints of mice were determined.Results: The paw edema score at 18-30 d and the paw arthritis score at 12-30 d in CIA group were higher than those in control group, and the paw edema score and paw arthritis score at 24-30 d in NF-kB inhibitor group were lower than those in CIA group. mRNA levels of IL-1β, MMP-1, TNF-α in serum and TRAP, MMP-9, CtsK and β3-Integrin in joint tissues in CIA mice were higher than in controls. NF-κB inhibitor treatment significantly decreased the above mRNA levels both in serum and joint tissues.Conclusion: NF-κB pathway inhibition can ameliorate bone destruction in the foot joints of CIA mice, which may be related to the reduction of inflammatory bone destruction and osteoclastogenesis. Keywords: Collagen induced arthritis; osteoclasts; bone destruction; inflammatory response; interleukin-1β; nuclear factor κB

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