Effect of Taxifolin Glycoside on Atopic Dermatitis-Like Skin Lesions in NC/Nga Mice

被引:46
作者
Ahn, Ji Young
Choi, Sun Eun [2 ]
Jeong, Mi Sook
Park, Kwan Hee [2 ]
Moon, Nam Ju
Joo, Seong Soo [3 ]
Lee, Chung Soo
Choi, Young Wook [2 ]
Li, Kapsok
Lee, Mi-Kyung
Lee, Min Won [2 ]
Seo, Seong Jun [1 ]
机构
[1] Chung Ang Univ, Coll Med, Dept Dermatol, Seoul 156756, South Korea
[2] Chung Ang Univ, Coll Pharm, Seoul 156756, South Korea
[3] Chungbuk Natl Univ, Vet Med Res Inst, Cheongju 361763, South Korea
关键词
Rhododendron mucronulatum; flavonoid; taxifolin; 3-O-beta-D-glucopyranoside; Th2; atopic dermatitis; EOSINOPHILS; CHEMOKINES; EXTRACT; CELLS;
D O I
10.1002/ptr.3084
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Increased levels of eosinphils, IgE, IL-4, 5, and 13 and pro-inflammatory factors (COX-2, iNOS) are observed in patients with atopic dermatitis (AD). Taxifolin 3-O-beta-D-glucopyranoside (TAX) from the roots of Rhododendron mucronulatum (RM) was examined to determine whether its immunomodulatory effect was applicable for treating atopic dermatitis. A total of 7 groups of NC/Nga mice with AD were treated by topical application or intraperitoneal injection of TAX for 4 weeks. Follow-up evaluations were done to assess the changes in clinical observations, eosinophil counts, and levels of IgE, cytokines, COX-2 and iNOS. In the clinical observation during the experimental period, TAX treatment significantly reduced the severity of AD-like lesions induced in NC/Nga mice. Eosinophil and IgE levels decreased after treatment of the animals with TAX. TAX may thus be associated with improvement of eosinophil-related allergic diseases. The expression of cytokines (IL-4, 5 and 13) was significantly inhibited in the TAX-treated group, suggesting that TAX might play an immunoregulatory role associated with AD. In RT-PCR, iNOS and COX-2 expression levels were reduced in the TAX-treated group. In western blotting, the expression levels of iNOS and COX-2 were also reduced in the TAX-treated group. These findings suggest that TAX is effective for the treatment of AD by preventing the production of inflammatory cytokines and by reducing skin inflammation. Copyright (C) 2009 John Wiley & Sons, Ltd.
引用
收藏
页码:1071 / 1077
页数:7
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