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Syringaldehyde ameliorates mouse arthritis by inhibiting dendritic cell maturation and proinflammatory cytokine secretion. | LitMetric

Syringaldehyde ameliorates mouse arthritis by inhibiting dendritic cell maturation and proinflammatory cytokine secretion.

Int Immunopharmacol

Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi 830017, China. Electronic address:

Published: August 2023

AI Article Synopsis

  • Syringaldehyde (SD) is a flavonoid with antioxidant and anti-inflammatory properties, and its potential effects on rheumatoid arthritis (RA) treatment via dendritic cell (DC) modulation were studied.
  • The findings indicated that SD down-regulated markers associated with DC maturation and reduced pro-inflammatory cytokines while increasing IL-10 secretion, influencing the MAPK/NF-κB signaling pathways.
  • In mouse models of arthritis, SD reduced joint swelling and pro-inflammatory cytokine levels while promoting regulatory T cell (Tregs) generation and inhibiting the differentiation of inflammatory T cell subsets.

Article Abstract

Syringaldehyde (SD), a kind of flavonoid polyphenolic small molecule compound, has the antioxidant and anti-inflammatory properties. But it is unknown whether SD has properties on the treatment of rheumatoid arthritis (RA) by modulating dendritic cells (DCs). We explored the effect of SD on the maturation of DCs in vitro and in vivo. The results showed that SD significantly down-regulated the expression of CD86, CD40 and MHC II, decreased the secretion of TNF-α, IL-6, IL-12p40 and IL-23, and increased IL-10 secretion and antigen phagocytosis in vitro induced by lipopolysaccharides in a dose-dependent manner through reducing the activation of MAPK/NF-κB signaling pathways. SD also significantly inhibited the expression of CD86, CD40 and MHC II on DCs in vivo. Moreover, SD suppressed the expression of CCR7 and the in vivo migration of DCs. In arthritis mouse models induced by λ-carrageenan and complete Freund's adjuvant, SD significantly alleviated paw and joint oedema, reduced the levels of pro-inflammatory cytokines TNF-α and IL-6 and increased the level of IL-10 in serum. Interestingly, SD significantly decreased the numbers of type I helper T cells (Th1), Th2, Th17 and Th17/Th1-like (CD4IFN-γIL-17A), but increased the numbers of regulatory T cells (Tregs) in spleens of mice. Importantly, the numbers of CD11cIL-23 and CD11cIL-6 cells were negatively correlated with the numbers of Th17 and Th17/Th1-like. These results suggested that SD ameliorated mouse arthritis through inhibiting the differentiation of Th1, Th17 and Th17/Th1-like and promoting the generation of Tregs via regulation of DC maturation.

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Source
http://dx.doi.org/10.1016/j.intimp.2023.110490DOI Listing

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