کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2541851 1122677 2010 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Hirsutenone inhibits lipopolysaccharide-activated NF-κB-induced inflammatory mediator production by suppressing Toll-like receptor 4 and ERK activation
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی ایمونولوژی
پیش نمایش صفحه اول مقاله
Hirsutenone inhibits lipopolysaccharide-activated NF-κB-induced inflammatory mediator production by suppressing Toll-like receptor 4 and ERK activation
چکیده انگلیسی

Microbial products, including lipopolysaccharide, may be involved in the pathogenesis of skin diseases such as atopic dermatitis. Diarylheptanoids such as oregonin and hirsutenone have been shown to have an anti-inflammatory effect. We investigated the effect of hirsutenone on lipopolysaccharide-induced inflammatory mediator production in keratinocytes in relation to the Toll-like receptor 4-mediated activation of the extracellular signal-regulated kinase (ERK) and nuclear factor (NF)-κB pathways. Hirsutenone, dexamethasone, ERK inhibitor or Bay 11-7085 (an inhibitor of NF-κB activation) reduced the lipopolysaccharide-induced production of cytokines IL-1β and IL-8, and the chemokine CCL17. Hirsutenone, ERK inhibitor or Bay 11-7085 also prevented the lipopolysaccharide-induced expression of Toll-like receptor 4, the phosphorylation of inhibitory κB-α, the activation of NF-κB and the expression of ERK. The results show that hirsutenone may reduce the lipopolysaccharide-stimulated production of inflammatory mediators in keratinocytes by suppressing the Toll-like receptor 4 expression-mediated NF-κB activation that is regulated by the ERK pathway. These findings suggest that hirsutenone may exert a preventive effect against microbial endotoxin lipopolysaccharide-induced inflammatory skin diseases through inhibition of ERK pathway-mediated NF-κB activation.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: International Immunopharmacology - Volume 10, Issue 4, April 2010, Pages 520–525
نویسندگان
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