Mangiferin corrects the imbalance of Th17/Treg cells in mice with TNBS-induced colitis

Int Immunopharmacol. 2016 May:34:220-228. doi: 10.1016/j.intimp.2016.03.004. Epub 2016 Mar 9.

Abstract

In the previous study, 80% ethanol extract of the rhizome mixture of Anemarrhena asphodeloides and Coptidis chinensis (AC) and its main constituent mangiferin improved TNBS-induced colitis in mice by inhibiting macrophage activation related to the innate immunity. In the preliminary study, we found that AC could inhibit Th17 cell differentiation in mice with TNBS-induced colitis. Therefore, we investigated whether AC and it main constituent mangiferin are capable of inhibiting inflammation by regulating T cell differentiation related to the adaptive immunity in vitro and in vivo. AC and mangiferin potently suppressed colon shortening and myeloperoxidase activity in mice with TNBS-induced colitis. They also suppressed TNBS-induced Th17 cell differentiation and IL-17 expression, but increased TNBS-suppressed Treg cell differentiation and IL-10 expression. Moreover, AC and mangiferin strongly inhibited the expression of TNF-α and IL-17, as well as the activation of NF-κB. Furthermore, mangiferin potently inhibited the differentiation of splenocytes into Th7 cells and increased the differentiation into Treg cells in vitro. Mangiferin also inhibited RORγt and IL-17 expression and STAT3 activation in splenocytes and induced Foxp3 and IL-10 expression and STAT5 activation. Based on these findings, mangiferin may ameliorate colitis by the restoration of disturbed Th17/Treg cells and inhibition of macrophage activation.

Keywords: Colitis; Macrophage; Mangiferin; Th17 cell; Treg cell.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anemarrhena / immunology
  • Animals
  • Cell Differentiation / drug effects
  • Cells, Cultured
  • Colitis / chemically induced
  • Colitis / drug therapy*
  • Colitis / immunology
  • Coptis chinensis
  • Drugs, Chinese Herbal / therapeutic use*
  • Forkhead Transcription Factors / metabolism
  • Homeostasis
  • Humans
  • Interleukin-10 / genetics
  • Interleukin-10 / metabolism
  • Interleukin-17 / genetics
  • Interleukin-17 / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • NF-kappa B / metabolism
  • Nuclear Receptor Subfamily 1, Group F, Member 3 / genetics
  • Nuclear Receptor Subfamily 1, Group F, Member 3 / metabolism
  • T-Lymphocytes, Regulatory / drug effects*
  • T-Lymphocytes, Regulatory / immunology
  • Th17 Cells / drug effects*
  • Th17 Cells / immunology
  • Trinitrobenzenesulfonic Acid
  • Xanthones / therapeutic use*

Substances

  • Drugs, Chinese Herbal
  • Forkhead Transcription Factors
  • Foxp3 protein, mouse
  • Interleukin-17
  • NF-kappa B
  • Nuclear Receptor Subfamily 1, Group F, Member 3
  • Xanthones
  • Interleukin-10
  • mangiferin
  • Trinitrobenzenesulfonic Acid
  • Coptidis rhizoma extract