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Dieckol, a Component of Ecklonia cava, Suppresses the Production of MDC/CCL22 via Down-Regulating STAT1 Pathway in Interferon-γ Stimulated HaCaT Human Keratinocytes

  • Kang, Na-Jin (Department of Biomedicine & Drug Development, School of Medicine, Jeju National University) ;
  • Koo, Dong-Hwan (Department of Biomedicine & Drug Development, School of Medicine, Jeju National University) ;
  • Kang, Gyeoung-Jin (Department of Medicine, School of Medicine, Jeju National University) ;
  • Han, Sang-Chul (Department of Medicine, School of Medicine, Jeju National University) ;
  • Lee, Bang-Won (Department of Medicine, School of Medicine, Jeju National University) ;
  • Koh, Young-Sang (Department of Biomedicine & Drug Development, School of Medicine, Jeju National University) ;
  • Hyun, Jin-Won (Department of Biomedicine & Drug Development, School of Medicine, Jeju National University) ;
  • Lee, Nam-Ho (Department of Chemistry, College of Natural Science, Jeju National University) ;
  • Ko, Mi-Hee (Jeju Biodiversity Research Institute) ;
  • Kang, Hee-Kyoung (Department of Biomedicine & Drug Development, School of Medicine, Jeju National University) ;
  • Yoo, Eun-Sook (Department of Biomedicine & Drug Development, School of Medicine, Jeju National University)
  • 투고 : 2014.12.15
  • 심사 : 2015.02.26
  • 발행 : 2015.05.01

초록

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-${\gamma}$ (IFN-${\gamma}$)-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-${\gamma}$ (10 ng/mL) in a dose dependent manner. Dieckol (5 and $10{\mu}M$) 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.

키워드

과제정보

연구 과제 주관 기관 : National Research Foundation of Korea

참고문헌

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