3,4,5-tricaffeoylquinic Acid inhibits the lipopolysaccharide-stimulated production of inflammatory mediators in keratinocytes

Pharmacology. 2012;90(3-4):183-92. doi: 10.1159/000342127. Epub 2012 Aug 29.

Abstract

Background and purpose: Microbial product lipopolysaccharide (LPS) has been shown to be involved in the pathogenesis of inflammatory skin diseases. Caffeoyl derivatives have demonstrated anti-inflammatory and antioxidant effects. However, the effect of 3,4,5-tricaffeoylquinic acid (3,4,5-triCQA) on the production of microbial product-induced inflammatory mediators in keratinocytes has not yet been studied.

Experimental approach: Using human keratinocytes, we investigated the effect of 3,4,5-triCQA on the LPS-stimulated production of inflammatory mediators in relation to the nuclear factor (NF)-ĸB, Akt and ERK pathways.

Results: 3,4,5-triCQA inhibited the LPS-induced expression of Toll-like receptor 4, and the production of cytokines and chemokines in keratinocytes. 3,4,5-triCQA, Bay 11-7085, Aĸt inhibitor and ERK inhibitor each attenuated the LPS-induced production of inflammatory mediators by inhibiting the NF-ĸB, Akt and ERK pathways.

Conclusions and implications: 3,4,5-triCQA may attenuate the LPS-stimulated production of inflammatory mediators in keratinocytes by suppressing the Toll-like receptor 4 expression-mediated activation of the Akt, ERK and NF-ĸB pathways. 3,4,5-triCQA may exert a preventive effect against microbial product-induced inflammatory skin diseases.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Survival / drug effects
  • Cells, Cultured
  • Chlorogenic Acid / analogs & derivatives*
  • Chlorogenic Acid / pharmacology
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Humans
  • Inflammation Mediators / metabolism*
  • Keratinocytes / metabolism*
  • Lipopolysaccharides / antagonists & inhibitors*
  • NF-kappa B / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Quinic Acid / analogs & derivatives

Substances

  • Inflammation Mediators
  • Lipopolysaccharides
  • NF-kappa B
  • caffeoylquinic acid
  • Quinic Acid
  • Chlorogenic Acid
  • Proto-Oncogene Proteins c-akt
  • Extracellular Signal-Regulated MAP Kinases