Isoliquiritigenin prevents the progression of psoriasis-like symptoms by inhibiting NF-κB and proinflammatory cytokines

J Mol Med (Berl). 2016 Feb;94(2):195-206. doi: 10.1007/s00109-015-1338-3. Epub 2015 Sep 18.

Abstract

Isoliquiritigenin (ISL) is an important flavonoid component of licorice and has been reported to possess anti-inflammatory and antioxidant properties, but its exact mechanism of action remains poorly understood. Previously, we demonstrated that ISL could suppress IL-6 expression in multiple myeloma. Here, we further characterized the anti-inflammatory effects of ISL in several psoriasis models, including the keratin 14/vascular endothelial growth factor (VEGF) transgenic mouse, the imiquimod (IMQ)-induced psoriasis-like mouse, and the human keratinocytes HaCaT and NHEK in vitro. We found that ISL ameliorated the inflammatory process in psoriasis models but not in their respective controls. Moreover, the anti-inflammatory effects of ISL were attributed to the suppression of nuclear factor-κB (NF-κB) activity, which consequently resulted in the reduction of pro-inflammation cytokines IL-6 and IL-8 expression. In conclusion, ISL exhibited anti-inflammatory effects in psoriasis models, by downregulating IL-6 and IL-8 via suppression of NF-κB activity, suggesting that ISL might serve as a potential candidate for treatment of psoriasis and other autoimmune inflammatory diseases.

Key message: ISL could ameliorate the inflammatory process of psoriasis. ISL could suppress NF-κB and subsequent production of a series of pro-inflammatory cytokines. Dual-inhibitory activity against IL-6 and IL-8 of ISL is implemented via inhibiting NF-κB. ISL exerts no inhibitory effects on normal human keratinocytes or wild-type Balb/c mice, implying its low toxicity and safety.

Keywords: Cytokines; Isoliquiritigenin; NF-κB; Psoriasis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Biomarkers
  • Cell Line
  • Cell Proliferation / drug effects
  • Chalcones / pharmacology*
  • Cytokines / metabolism*
  • Disease Models, Animal
  • Disease Progression
  • Dose-Response Relationship, Drug
  • Female
  • Humans
  • Immunohistochemistry
  • Inflammation Mediators / metabolism*
  • Keratinocytes / drug effects
  • Keratinocytes / metabolism
  • Mice
  • Mice, Transgenic
  • NF-kappa B / metabolism*
  • Psoriasis / drug therapy
  • Psoriasis / genetics
  • Psoriasis / metabolism*
  • Psoriasis / pathology*
  • Skin / immunology
  • Skin / metabolism
  • Skin / pathology

Substances

  • Biomarkers
  • Chalcones
  • Cytokines
  • Inflammation Mediators
  • NF-kappa B
  • isoliquiritigenin