Biomol Ther.
2015 May;23(3):238-244. 10.4062/biomolther.2014.141.
Dieckol, a Component of Ecklonia cava, Suppresses the Production of MDC/CCL22 via Down-Regulating STAT1 Pathway in Interferon-gamma Stimulated HaCaT Human Keratinocytes
- Affiliations
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- 1Department of Biomedicine & Drug Department, School of Medicine, Jeju National University, Jeju 690-756, Republic of Korea. eunsyoo@jejunu.ac.kr
- 2Department of Medicine, School of Medicine, Jeju National University, Jeju 690-756, Republic of Korea.
- 3Department of Chemistry, College of Natural Science, Jeju National University, Jeju 690-756, Republic of Korea.
- 4Jeju Biodiversity Research Institute, JejuTechnopark, Jeju 699-943, Republic of Korea.
- KMID: 2380333
- DOI: http://doi.org/10.4062/biomolther.2014.141
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.
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