کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2541851 | 1122677 | 2010 | 6 صفحه PDF | دانلود رایگان |

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.
Journal: International Immunopharmacology - Volume 10, Issue 4, April 2010, Pages 520–525