Suppression of thymus- and activation-regulated chemokine (TARC/CCL17) production by 1,2,3,4,6-penta-O-galloyl-β-d-glucose via blockade of NF-κB and STAT1 activation in the HaCaT cells

Ju, Sung Mi; Song, Ha Yong; Lee, Su Jin; Seo, Won Yong; Sin, Dong Hyeon; Goh, Ah Ra; Kang, Young‐Hee; Kang, Inhye; Won, Moo‐Ho; Yi, Jae-Seon; Kwon, Dong-Joo; Bae, Young-Soo; Choi, Soo Young; Park, Jinseu

doi:10.1016/j.bbrc.2009.06.137

Cited by 72 publications

(68 citation statements)

References 23 publications

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“…IFN-γ and TNF-α induces the production of chemokines in keratinocytes through activation of STAT1 and NF-κB (Ju et al, 2009). Therefore, we examined the effect of SFN on the activation of STAT1 and NF-κB that was required for the production of TARC/ CCL17 and MDC/CCL22 in HaCaT cells.…”

Section: Effect Of Sfn On Stat1 and Nf-κb Activation Induced By Ifn-γmentioning

confidence: 99%

Sulforaphane suppresses TARC/CCL17 and MDC/CCL22 expression through heme oxygenase-1 and NF-κB in human keratinocytes

Jeong¹,

Choi

Jang

2010

Arch. Pharm. Res.

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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-κB 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-γ (IFN-γ) and tumor necrosis factor (TNF)-α- induced thymus- and activation-regulated chemokine (TARC/CCL17) and macrophage-derived chemokine (MDC/CCL22) production in HaCaT keratinocytes. SFN inhibited IFN-γ and TNF-α-induced NF-κB activation as well as STAT1 activation. Interestingly, pretreatment with SFN result in significantly suppressed IFN-γ and TNF-α-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-γ and TNF-α-induced TARC/CCL17 and MDC/CCL22 production. These results demonstrate that SFN has an inhibitory role in IFN-γ and TNF-α-induced production of TARC/CCL17 and MDC/CCL22 in human HaCaT cells by inhibition of NF-κB activation and induction of HO-1.

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Section: Effect Of Sfn On Stat1 and Nf-κb Activation Induced By Ifn-γmentioning

confidence: 99%

Sulforaphane suppresses TARC/CCL17 and MDC/CCL22 expression through heme oxygenase-1 and NF-κB in human keratinocytes

Jeong¹,

Choi

Jang

2010

Arch. Pharm. Res.

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“…However, prolonged use of steroid has side effects such as thinning of the skin, leading to cracking and bleeding [21]. Natural compounds from herbs and plants are potential sources of therapeutic agents for preventing and treating inflammatory skin diseases [22][23][24]. The phytosterol 3-O-b-D-glucopyranosylspinasterol (spinasterol-Glc) from Stewartia koreana leaf extracts is strongly anti-inflammatory and inhibits production of CCL17 in keratinocytes [25,26].…”

Section: Introductionmentioning

confidence: 99%

Inhibitory effect of 5,6-dihydroergosteol-glucoside on atopic dermatitis-like skin lesions via suppression of NF-κB and STAT activation.

Jung

Lee

et al. 2015

Journal of Dermatological Science

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“…Studies have shown that STAT and/or NF-κB activation are mediated by TNF-α and/ or IFN-γ in keratinocytes. [9][10][11][12] Because the promoters of MDC, and RANTES contain STAT-and NF-κB-binding sites, 34,35) it is possible that chemokine production can be regulated via activation of the STAT1 and NF-κB pathways. We found that TNF-α and IFN-γ treatment increased the level of phospho-STAT1 in HaCaT cells, whereas treatment with GJBRH extract markedly reduced this phosphorylation of STAT1 (Figs.…”

Section: Discussionmentioning

confidence: 99%

“…Among the members of the STAT family proteins, STAT1 plays a critical role in the regulation of primary inflammatory responses. 7,8) In keratinocytes, STAT1 is a pivotal regulator of the IFN-γ and/or TNF-α-stimulated immune responses [9][10][11][12] and eventually stimulate the production of chemokines, including TARC, MDC, and RANTES. 13,14) Thus, STAT1 is considered an important molecule for studying inflammatory disorders of skin, including atopic dermatitis.…”

mentioning

confidence: 99%

Anti-inflammatory Actions of Herbal Formula Gyejibokryeong-Hwan Regulated by Inhibiting Chemokine Production and STAT1 Activation in HaCaT Cells

Jeong

Lim

Seo

et al. 2015

Biological & Pharmaceutical Bulletin

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Gyejibokryeong-hwan (GJBRH; Keishi-bukuryo-gan in Japan and Guizhi Fuling Wan in China) is a traditional herbal formula comprising five medicinal herbs and is used to treat climacteric syndrome. GJBRH has been shown to exhibit biological activity against diabetes, diabetic nephropathy, atherosclerosis, ischemia, and cancer. However, there is no scientific evidence of its activities against skin inflammation, including atopic dermatitis. We used the HaCaT human keratinocyte cell line to investigate the effects of GJBRH on skin inflammation. No significant cytotoxicity was observed in cells treated with GJBRH up to a concentration of 1000 µg/mL. Exposure to the proinflammatory cytokines tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ) significantly increased HaCaT cell production of the following chemokines: macrophage-derived chemokine (

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Suppression of thymus- and activation-regulated chemokine (TARC/CCL17) production by 1,2,3,4,6-penta-O-galloyl-β-d-glucose via blockade of NF-κB and STAT1 activation in the HaCaT cells

Cited by 72 publications

References 23 publications

Sulforaphane suppresses TARC/CCL17 and MDC/CCL22 expression through heme oxygenase-1 and NF-κB in human keratinocytes

Sulforaphane suppresses TARC/CCL17 and MDC/CCL22 expression through heme oxygenase-1 and NF-κB in human keratinocytes

Inhibitory effect of 5,6-dihydroergosteol-glucoside on atopic dermatitis-like skin lesions via suppression of NF-κB and STAT activation.

Anti-inflammatory Actions of Herbal Formula Gyejibokryeong-Hwan Regulated by Inhibiting Chemokine Production and STAT1 Activation in HaCaT Cells

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