Curcumin inhibits imiquimod-induced psoriasis-like inflammation by inhibiting IL-1beta and IL-6 production in mice

PLoS One. 2013 Jun 25;8(6):e67078. doi: 10.1371/journal.pone.0067078. Print 2013.

Abstract

Curcumin, a selective phosphorylase kinase inhibitor, is a naturally occurring phytochemical present in turmeric. Curcumin has been confirmed to have anti-inflammatory properties in addition to the ability to decrease the expression of pro-inflammatory cytokines in keratinocytes. The interleukin-23 (IL-23)/IL-17A cytokine axis plays a critical role in the pathogenesis of psoriasis. Here, we report that topical use of a curcumin gel formulation strongly inhibited imiquimod (IMQ)-induced psoriasis-like inflammation, the development of which was based on the IL-23/IL-17A axis. IMQ-induced epidermal hyperplasia and inflammation in BALB/c mouse ear was significantly inhibited following curcumin treatment. Real-time PCR showed that mRNA levels of IL-17A, IL-17F, IL-22, IL-1β, IL-6 and TNF-α cytokines were decreased significantly by curcumin in ear skin, an effect similar to that of clobetasol. In addition, we found that curcumin may enhance the proliferation of epidermis γδ T cells but inhibit dermal γδ T cell proliferation. We inferred that curcumin was capable of impacting the IL-23/IL-17A axis by inhibiting IL-1β/IL-6 and then indirectly down-regulating IL-17A/IL-22 production. In conclusion, curcumin can relieve the IMQ-induced psoriasis-like inflammation in a mouse model, similar to the effects of clobetasol. Therefore, we have every reason to expect that curcumin will be used in the treatment of psoriasis in the future.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aminoquinolines / pharmacology*
  • Animals
  • Cell Proliferation / drug effects
  • Curcumin / pharmacology*
  • Curcumin / therapeutic use
  • Ear
  • Gene Expression Regulation / drug effects
  • Imiquimod
  • Inflammation / chemically induced
  • Inflammation / drug therapy
  • Inflammation / metabolism
  • Inflammation / pathology
  • Interleukin-1beta / biosynthesis*
  • Interleukin-6 / biosynthesis*
  • Mice
  • Mice, Inbred BALB C
  • Nuclear Receptor Subfamily 1, Group F, Member 3 / metabolism
  • Psoriasis / chemically induced*
  • Psoriasis / drug therapy*
  • Psoriasis / metabolism
  • Psoriasis / pathology
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Receptors, Antigen, T-Cell, gamma-delta / metabolism
  • Receptors, CCR6 / metabolism
  • Skin / drug effects
  • Skin / metabolism
  • Skin / pathology

Substances

  • Aminoquinolines
  • CCR6 protein, mouse
  • Interleukin-1beta
  • Interleukin-6
  • Nuclear Receptor Subfamily 1, Group F, Member 3
  • RNA, Messenger
  • Receptors, Antigen, T-Cell, gamma-delta
  • Receptors, CCR6
  • Curcumin
  • Imiquimod

Grant support

This study was supported financially by Grant 30873128 from the National Natural Science Foundation of China. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.