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KMID : 0043320100330111867
Archives of Pharmacal Research
2010 Volume.33 No. 11 p.1867 ~ p.1876
Sulforaphane suppresses TARC/CCL17 and MDC/CCL22 expression through heme oxygenase-1 and NF-¥êB in human keratinocytes
Jeong Seung-Il

Choi Byung-Min
Jang Seon-Il
Abstract
Sulforaphane (4-methylsulfinylbutyl isothiocyanate, SFN) from broccoli has been used a chemopreventive photochemical as detoxification of xenobiotics and anti-inflammatory, however, there is no studies for Th2 chemokine expression through heme oxygenase-1 and NF-¥êB in keratinocytes. Atopic dermatitis is a chronically relapsing pruritic inflammatory skin disease. SFN is demonstrated to have anti-inflammatory and anti-oxidant effects. This study aimed to define whether and how SFN regulates Th2-related chemokine production in human HaCaT keratinocytes. The level of chemokine expression was measured by reverse transcription polymerase chain reaction (RT-PCR) and signaling study was performed by Western blot analysis. Chemokine production was determined by enzyme-linked immunosorbent assay. Pretreatment with SFN suppressed interferon-¥ã (IFN-¥ã) and tumor necrosis factor (TNF)-¥á- induced thymus- and activation-regulated chemokine (TARC/CCL17) and macrophage-derived chemokine (MDC/CCL22) production in HaCaT keratinocytes. SFN inhibited IFN-¥ã and TNF-¥á-induced NF-¥êB activation as well as STAT1 activation. Interestingly, pretreatment with SFN result in significantly suppressed IFN-¥ã and TNF-¥á-induced TARC/CCL17 and MDC/CCL22 production through the induction of HO-1. This suppression was completely abolished by HO-1 siRNA. Furthermore, Carbon monoxide, but not other end products of HO-1 activity, also suppressed IFN-¥ã and TNF-¥á-induced TARC/CCL17 and MDC/CCL22 production. These results demonstrate that SFN has an inhibitory role in IFN-¥ã and TNF-¥á-induced production of TARC/CCL17 and MDC/CCL22 in human HaCaT cells by inhibition of NF-¥êB activation and induction of HO-1.
KEYWORD
Sulforaphane, Th2 chemokines, Heme oxygenase-1, NF-¥êB
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