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DW2007 Ameliorates Colitis and Rheumatoid Arthritis in Mice by Correcting Th17/Treg Imbalance and Inhibiting NF-κB Activation

  • Lim, Su-Min (Department of Life and Nanopharmaceutical Sciences and Department of Pharmacy, Kyung Hee University) ;
  • Lee, Sang-Yun (Department of Life and Nanopharmaceutical Sciences and Department of Pharmacy, Kyung Hee University) ;
  • Jeong, Jin-Ju (Department of Life and Nanopharmaceutical Sciences and Department of Pharmacy, Kyung Hee University) ;
  • Choi, Hyun Sik (DongWha Pharm Research Institute) ;
  • Chang, Hwan Bong (DongWha Pharm Research Institute) ;
  • Kim, Dong-Hyun (Department of Life and Nanopharmaceutical Sciences and Department of Pharmacy, Kyung Hee University)
  • Received : 2016.01.27
  • Accepted : 2016.03.24
  • Published : 2016.11.01

Abstract

In the previous study, the rhizome mixture of Anemarrhena asphodeloides and Coptis chinensis (DW2007), improved TNBS-, oxazolone-, or DSS-induced colitis in mice by regulating macrophage activation. Therefore, to understand the effect of DW2007 on the T cell differentiation involved in the adaptive immunity, we measured its effect on both Th17 and Treg cell differentiation in splenocytes, in the lamina propria of mice with DSS-induced colitis (DIC), and in the spleens of mice with collagen-induced arthritis (CIA). Results showed that DW2007 potently inhibited the differentiation of splenocytes into Th17 cells, but increased Treg cell differentiation in vitro. In the colon of wild type and $TLR4^{-/-}$ mice with DIC, DW2007 potently suppressed DSS-induced colon shortening and myeloperoxidase activity. DW2007 also suppressed collagen-induced paw thickening, clinical index, and myeloperoxidase activity in CIA mice. Overall, DW2007 potently suppressed Th17 cell differentiation in mice with CIA and DIC, but increased Treg cell differentiation. Moreover, DW2007 strongly inhibited the expression of TNF-${\alpha}$ and IL-$1{\beta}$, as well as the activation of NF-${\kappa}B$. Based on these findings, DW2007 may ameliorate inflammatory diseases by regulating the innate immunity via the inhibition of macrophage activation and the adaptive immunity via the correction of disturbed Th17/Treg cells.

Keywords

References

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