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

We first examined the cell cytotoxicity of eckol and dieckol against HaCaT cells. The cells were treated with different concentrations of eckol and dieckol (12.5, 25, and 50 mM) for 24 h. Cell viability was determined using an EZ-cytox-enhanced cell viability assay kit. As shown in Fig. 2A and 2C, eckol and dieckol did not exhibit cytotoxicity to HaCaT keratinocytes at the tested concentrations. Then, we evaluated the inhibitory effects of eckol and dieckol on inflammatory chemokine (MDC) production in IFN-γ (10 ng/mL)-stimulated HaCaT keratinocytes. The basal level of MDC production is 118.0 ± 8.3 pg/ mL, and 278.6 ± 6.0 pg/mL of MDC was produced by IFN-γ treatment (10 ng/mL). Interestingly, eckol failed to inhibit the cytokine-stimulated production of MDC (Fig. 2B) . However, dieckol significantly suppressed the production of MDC by IFN-γ in a concentration-dependent manner. Especially, 12.5 uM dieckol strongly suppressed by 135 ± 12.7 pg/mL (almost the basal level) of MDC production in IFN-γ-stimulated HaCaT keratinocyte (Fig. 2D ).