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Aloperine Ameliorates IMQ-Induced Psoriasis by Attenuating Th17 Differentiation and Facilitating Their Conversion to Treg

  • Hai Feng Zhou
  • , Fa Xi Wang
  • , Fei Sun
  • , Xin Liu
  • , Shan Jie Rong
  • , Jia Hui Luo
  • , Tian Tian Yue
  • , Jun Xiao
  • , Chun Liang Yang
  • , Wan Ying Lu
  • , Xi Luo
  • , Qing Zhou
  • , He Zhu
  • , Ping Yang
  • , Fei Xiong
  • , Qi Lin Yu
  • , Shu Zhang*
  • , Cong Yi Wang*
  • *Corresponding author for this work
  • Huazhong University of Science and Technology

Research output: Contribution to journalArticlepeer-review

Abstract

Aloperine is an anti-inflammatory compound isolated from the Chinese herb Sophora alopecuroides L. Previously, our group has reported that the generation of induced Treg was promoted by aloperine treatment in a mouse colitis model. However, the effect of aloperine on effector T cell subsets remains unclear. We therefore carefully examined the effect of aloperine on the differentiation of major subsets of T helper cells. Based on our results, psoriasis, a Th17 dominant skin disease, is selected to explore the potential therapeutic effect of aloperine in vivo. Herein, we demonstrated that topical application of aloperine suppressed epidermal proliferation, erythema, and infiltration of inflammatory cells in skin lesions. Mechanistic studies revealed that aloperine suppressed the differentiation of Th17 cells directly through inhibiting the phosphorylation of STAT3 or indirectly through impairing the secretion of Th17-promoting cytokines by dendritic cells. Moreover, aloperine enhanced the conversion of Th17 into Treg via altering the pSTAT3/pSTAT5 ratio. Collectively, our study supported that aloperine possesses the capacity to affect Th17 differentiation and modulates Th17/Treg balance, thereby alleviating imiquimod (IMQ)-induced psoriasis in mice.

Original languageEnglish
Article number778755
JournalFrontiers in Pharmacology
Volume13
DOIs
Publication statusPublished - 1 Jun 2022
Externally publishedYes

Keywords

  • Aloperine
  • Psoriasis
  • STAT3/STAT5 pathway
  • Th17 differentiation
  • Th17 to Treg conversion

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