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

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

The MAPK pathway is reportedly involved in the production of inflammatory chemokines. Several plant extracts and compounds have been shown to inhibit the actions of inflammatory chemokines via the regulation of mitogen-activated protein kinase (MAPK) cascades. (Pearson et al., 2001; Madonna et al., 2008; Chae et al., 2013; Yoon et al., 2013) . To determine whether the MAPKs (ERK, JNK, p38) signaling is involved in IFN-γ induced MDC production in HaCaT cells, we first examined time dependent activation of three MAPKs (ERK, JNK, p38) after IFN-γ treatment. IFN-γ induced the phosphorylation of ERK at 5 min, while did not affect on the phosphorylation of JNK and P-38. Then, we focused on the inhibitory effect of dieckol on the ERK activation in IFN-γ-stimulated HaCaT cells, but, the effect of dieckol was not significant. To confirm whether MAPKs pathway associate with MDC production, we determined the MDC levels after the treatment of known MAPKs inhibitors in IFN-γ-stimulated HaCaT cells. SP600125 (a specific JNK inhibitor) and PD98059 (a specific ERK inhibitor), and SB203580 (a specific p38 inhibitor) did not affect on the MDC production induced by IFN-γ. These results suggest that MAPKs pathway does not contribute significantly on the production of MDC in IFN-γ stimulated HaCaT cells.