Dieckol, a Component of Ecklonia cava, Suppresses the Production of MDC/CCL22 via Down-Regulating STAT1 Pathway in Interferon-gamma Stimulated HaCaT Human Keratinocytes.
10.4062/biomolther.2014.141
- Author:
Na Jin KANG
1
;
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
Author Information
1. Department of Biomedicine & Drug Department, School of Medicine, Jeju National University, Jeju 690-756, Republic of Korea. eunsyoo@jejunu.ac.kr
- Publication Type:Original Article
- Keywords:
Dieckol;
Inflammation;
Keratinocyte;
MDC/CCL22;
STAT1
- MeSH:
Chemokine CCL22;
Chemokines;
Dendritic Cells;
Dermatitis, Atopic;
Down-Regulation;
Humans;
Inflammation;
Interferon-gamma*;
Keratinocytes*;
Killer Cells, Natural;
Lymphocytes;
Monocytes;
Phosphorylation;
Skin;
Transducers
- From:Biomolecules & Therapeutics
2015;23(3):238-244
- CountryRepublic of Korea
- Language:English
-
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-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 muM) 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.