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Multi-glycoside of Tripterygium wilfordii Hook. f. ameliorates imiquimod-induced skin lesions through a STAT3-dependent mechanism involving the inhibition of Th17-mediated inflammatory responses

  • Authors:
    • Jingxia Zhao
    • Tingting Di
    • Yan Wang
    • Xin Liu
    • Daiying Liang
    • Guangzhong Zhang
    • Ping Li

  • View Affiliations

  • Published online on: July 11, 2016     https://doi.org/10.3892/ijmm.2016.2670
  • Pages: 747-757

  • Copyright: © Zhao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Multi-glycoside of Tripterygium wilfordii Hook. f.(GTW) possesses anti-inflammatory and immunosuppressive properties, and has been used as a traditional treatment for psoriasis for many years, although the underlying immunological mechanisms remain poorly understood. The T helper (Th)17 cell response is considered to play a major role in the pathogenesis of psoriasis. Th17 cells are implicated in the mechanism of pathogenesis of imiquimod (IMQ)‑induced skin inflammation. Using a mouse model, we demonstrated that GTW protected mice from developing psoriasis-like lesions induced by topical IMQ administration. This protection was associated with significantly decreased mRNA levels of Th17 cytokines such as interleukin (IL)-17A, IL-17F and IL-22 in mouse skin samples as well as fewer IL-17-secreting splenic CD4+ lymphocytes in IMQ-exposed mice. There were no significant effects on the proportion of CD4+ interferon (IFN)-γ+ T cells, CD4+IL-4+ T cells and CD4+CD25+Foxp3+ Treg cells in the spleen cells. Taken together with the unchanged mRNA levels of Th1 cytokine IFN-γ, Th2 cytokine IL-4 and Treg cytokine IL-10 in IMQ-exposed mouse skin following GTW administration, our findings suggest that the immunosuppressive effect of GTW in psoriasis is exerted mainly on Th17 cells, rather than on Th1, Th2 or Treg cells. Furthermore, we showed that GTW suppressed Th17 function through the inhibition of STAT3 phosphorylation. These results have the potential to pave the way for the use of GTW as an agent for the treatment of psoriasis.
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September-2016
Volume 38 Issue 3

Print ISSN: 1107-3756
Online ISSN:1791-244X

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  • Impact Factor: 5.4
  • Ranked Medicine Research and Experimental
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  • CiteScore: 10.7
  • CiteScore Rank: Q1: #35/328 Biochemistry, Genetics and Molecular Biology
  • Source Normalized Impact per Paper (SNIP): 0.994
  • SCImago Journal Rank (SJR): 0.922
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Spandidos Publications style
Zhao J, Di T, Wang Y, Liu X, Liang D, Zhang G and Li P: Multi-glycoside of Tripterygium wilfordii Hook. f. ameliorates imiquimod-induced skin lesions through a STAT3-dependent mechanism involving the inhibition of Th17-mediated inflammatory responses. Int J Mol Med 38: 747-757, 2016
APA
Zhao, J., Di, T., Wang, Y., Liu, X., Liang, D., Zhang, G., & Li, P. (2016). Multi-glycoside of Tripterygium wilfordii Hook. f. ameliorates imiquimod-induced skin lesions through a STAT3-dependent mechanism involving the inhibition of Th17-mediated inflammatory responses. International Journal of Molecular Medicine, 38, 747-757. https://doi.org/10.3892/ijmm.2016.2670
MLA
Zhao, J., Di, T., Wang, Y., Liu, X., Liang, D., Zhang, G., Li, P."Multi-glycoside of Tripterygium wilfordii Hook. f. ameliorates imiquimod-induced skin lesions through a STAT3-dependent mechanism involving the inhibition of Th17-mediated inflammatory responses". International Journal of Molecular Medicine 38.3 (2016): 747-757.
Chicago
Zhao, J., Di, T., Wang, Y., Liu, X., Liang, D., Zhang, G., Li, P."Multi-glycoside of Tripterygium wilfordii Hook. f. ameliorates imiquimod-induced skin lesions through a STAT3-dependent mechanism involving the inhibition of Th17-mediated inflammatory responses". International Journal of Molecular Medicine 38, no. 3 (2016): 747-757. https://doi.org/10.3892/ijmm.2016.2670