AI Article Synopsis
- Rheumatoid arthritis (RA) is a long-term inflammatory condition that leads to joint damage, and green-lipped mussel (GLM) shows promise in reducing inflammation related to RA, although the exact way it works is still not fully understood.
- In a study with collagen-induced arthritis (CIA) mice, oral administration of GLM led to a reduction in the severity of the disease and lowered inflammation markers compared to a control group.
- Additionally, GLM was found to decrease the presence of harmful immune cells and inhibit the formation of osteoclasts, suggesting its potential as a treatment to manage RA by targeting these detrimental processes.
Article Abstract
Rheumatoid arthritis (RA) is a chronic inflammatory disorder characterized by progressive joint destruction. Green-lipped mussel (GLM) has chondro-modulatory and anti-inflammatory properties, but the mechanism underlying the effect of GLM on RA is unclear. To investigate the roles of GLM on the pathogenesis of RA, we examined the effects of GLM in collagen-induced arthritis (CIA) mice and osteoclast differentiation. GLM was orally administrated CIA mice at 3 weeks after chicken type II collagen (CII) immunizations. GLM reduced arthritis severity and the histologic score of CIA mice compared to vehicle. The expression of proinflammatory cytokines (TNF-α, IL-1β, and IL-17) was decreased in the ankle joints of GLM-treated CIA mice. The expression of CD4+ IL-17+ cells decreased in ex vivo splenocytes and the spleens of GLM-treated CIA mice. Moreover, GLM inhibited TRAP+ multinucleated cells among mouse bone marrow-derived monocytes/macrophages (BMM), and the expression of osteoclast-related genes in mouse BMMs and human monocytes in vitro. These results suggest that GLM has potential as a therapeutic agent that can improve disease by controlling pathologic immune cells and osteoclastogenesis.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9858385 | PMC |
| http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0280601 | PLOS |
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