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