Chrysin alleviates imiquimod-induced psoriasis-like skin inflammation and reduces the release of CCL20 and antimicrobial peptides

Sci Rep. 2020 Feb 19;10(1):2932. doi: 10.1038/s41598-020-60050-1.

Abstract

Psoriasis is a common non-contagious chronic inflammatory skin lesion, with frequent recurrence. It mainly occurs due to aberrant regulation of the immune system leading to abnormal proliferation of skin cells. However, the pathogenic mechanisms of psoriasis are not fully understood. Although most of the current therapies are mostly efficient, the side effects can result in therapy stop, which makes the effectiveness of treatment strategies limited. Therefore, it is urgent and necessary to develop novel therapeutics. Here, we investigated the efficacy of chrysin, a plant flavonoid, which we previously reported to possess strong antioxidant and anti-inflammatory effects, against psoriasis-like inflammation. Our results revealed that chrysin significantly attenuated imiquimod-induced psoriasis-like skin lesions in mice, and improved imiquimod-induced disruption of skin barrier. Moreover, the TNF-α, IL-17A, and IL-22-induced phosphorylation of MAPK and JAK-STAT pathways, and activation of the NF-κB pathway were also attenuated by chrysin pretreatment of epidermal keratinocytes. Most importantly, chrysin reduced TNF-α-, IL-17A-, and IL-22-induced CCL20 and antimicrobial peptide release from epidermal keratinocytes. Thus, our findings indicate that chrysin may have therapeutic potential against inflammatory skin diseases. Our study provides a basis for further investigating chrysin as a novel pharmacologic agent and contributes to the academic advancement in the field of Chinese herbal medicine.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antimicrobial Cationic Peptides / metabolism*
  • Chemokine CCL20 / genetics
  • Chemokine CCL20 / metabolism*
  • Disease Models, Animal
  • Down-Regulation / drug effects
  • Epidermis / pathology
  • Flavonoids / chemistry
  • Flavonoids / pharmacology
  • Flavonoids / therapeutic use*
  • Humans
  • Hyperplasia
  • Imiquimod / adverse effects*
  • Inflammation / drug therapy*
  • Interleukin-17 / metabolism
  • Interleukin-22
  • Interleukins / metabolism
  • Keratinocytes / drug effects
  • Keratinocytes / metabolism
  • MAP Kinase Signaling System / drug effects
  • Male
  • Mice, Inbred BALB C
  • NF-kappa B / metabolism
  • Phosphorylation / drug effects
  • Psoriasis / chemically induced*
  • Psoriasis / drug therapy*
  • Psoriasis / pathology
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Skin / drug effects
  • Skin / pathology*
  • Skin / physiopathology
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Antimicrobial Cationic Peptides
  • Chemokine CCL20
  • Flavonoids
  • Interleukin-17
  • Interleukins
  • NF-kappa B
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • chrysin
  • Imiquimod