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Total glucosides of paeony inhibits Th1/Th17 cells via decreasing dendritic cells activation in rheumatoid arthritis.

Abstract
Total glucoside of paeony (TGP), an active compound extracted from paeony root, has been used in therapy for rheumatoid arthritis (RA). Th1 and Th17 cells are now believed to play crucial roles in the lesions of RA. However, the molecular mechanism of TGP in inhibition of Th1 and Th17 cells remains unclear. In this study, we found that TGP treatment significantly decreased percentage and number of Th1 and Th17 cells in collagen induced arthritis (CIA) mice. Consistently, treatment with TGP decreased expression of T-bet and RORγt as well as phosphorylation of STAT1 and STAT3. In particular, TGP treatment inhibited dendritic cells (DCs) maturation and reduced production of IL-12 and IL-6. Moreover, TGP-treatment RA patients showed shank population of matured DCs and IFN-γ-, IL-17-producing cells. Taken together, our results demonstrated that TGP inhibited maturation and activation of DCs, which led to impaired Th1 and Th17 differentiation in vivo.
AuthorsJinpiao Lin, Lianbo Xiao, Guilin Ouyang, Yu Shen, Rongfen Huo, Zhou Zhou, Yue Sun, Xianjin Zhu, Jie Zhang, Baihua Shen, Ningli Li
JournalCellular immunology (Cell Immunol) Vol. 280 Issue 2 Pg. 156-63 (Dec 2012) ISSN: 1090-2163 [Electronic] Netherlands
PMID23399842 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2013 Elsevier Inc. All rights reserved.
Chemical References
  • Glucosides
  • Interleukin-6
  • STAT1 Transcription Factor
  • STAT3 Transcription Factor
  • Interleukin-12
Topics
  • Adult
  • Aged
  • Animals
  • Arthritis, Experimental (drug therapy, metabolism)
  • Arthritis, Rheumatoid (drug therapy, immunology, metabolism)
  • Dendritic Cells (drug effects, immunology)
  • Female
  • Glucosides (pharmacology)
  • Humans
  • Interleukin-12 (biosynthesis)
  • Interleukin-6 (biosynthesis)
  • Male
  • Mice
  • Mice, Inbred DBA
  • Middle Aged
  • Paeonia (chemistry)
  • STAT1 Transcription Factor (metabolism)
  • STAT3 Transcription Factor (metabolism)
  • Th1 Cells (drug effects)
  • Th17 Cells (drug effects)

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