Dieckol, a component of ecklonia cava, suppresses the production of MDC/CCL22 via down-regulating STAT1 pathway in interferon-γ stimulated HaCaT human keratinocytes

Na Jin Kang, Dong Hwan Koo, Gyeoung Jin Kang, Sang Chul Han, Bang Won Lee, Young Sang Koh, Jin Won Hyun, Nam Ho Lee, Mi Hee Ko, Hee Kyoung Kang, Eun Sook Yoo

Research output: Contribution to journalArticlepeer-review

16 Scopus citations

Abstract

Macrophage-derived chemokine, C-C motif chemokine 22 (MDC/CCL22), is one of the inflammatory chemokines that controls the movement of monocytes, monocyte-derived dendritic cells, and natural killer cells. Serum and skin MDC/CCL22 levels are elevated in atopic dermatitis, which suggests that the chemokines produced from keratinocytes are responsible for attracting inflammatory lymphocytes to the skin. A major signaling pathway in the interferon-γ (IFN-γ)-stimulated inflammation response involves the signal transducers and activators of transcription 1 (STAT1). In the present study, we investigated the anti-inflammatory effect of dieckol and its possible action mechanisms in the category of skin inflammation including atopic dermatitis. Dieckol inhibited MDC/CCL22 production induced by IFN-γ (10 ng/mL) in a dose dependent manner. Dieckol (5 and 10 μM) suppressed the phosphorylation  and the nuclear translocation of STAT1. These results suggest that dieckol exhibits anti-inflammatory effect via the down-regulation of STAT1 activation.

Original languageEnglish (US)
Pages (from-to)238-244
Number of pages7
JournalBiomolecules and Therapeutics
Volume23
Issue number3
DOIs
StatePublished - 2015

Keywords

  • Dieckol
  • Inflammation
  • Keratinocyte
  • MDC/CCL22
  • STAT1

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