Therapeutic effects of Baicalein on atopic dermatitis-like skin lesions of NC/Nga mice induced by dermatophagoides pteronyssinus

被引:57
|
作者
Yun, Mi-Young [7 ]
Yang, Jae-Heon [6 ]
Kim, Dae-Keun [6 ]
Cheong, Kwang-Jo [5 ]
Song, Hyang-Hee [5 ]
Kim, Dong-Hee [4 ]
Cheong, Kyu-Jin [3 ]
Kim, Young-Il [2 ]
Shin, Sang-Chul [1 ]
机构
[1] Chonnam Natl Univ, Coll Pharm, Kwangju 500757, South Korea
[2] Konyang Univ, Dept Pharmaceut Engn, Nonsan 320711, South Korea
[3] Chungnam Natl Univ, Coll Pharm, Taejon 305764, South Korea
[4] Daejeon Univ, Coll Oriental Med, Dept Pathol, Taejon 300716, South Korea
[5] Daejeon Univ, Dept Beauty Hlth Care, Taejon 300716, South Korea
[6] Woosuk Univ, Dept Pharm, Samrye 565701, South Korea
[7] Byuksung Coll, Dept Hlth Welf, Gimje 576711, South Korea
关键词
(BE); Baicalein; (AD); Atopic dermatitis; NC/Nga mice; Inflammatory cytokines; Immune cells; TOPICAL APPLICATION; EXPRESSION; MOUSE; MODEL;
D O I
10.1016/j.intimp.2010.06.020
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The present study was conducted to investigate the effects of Baicalein (BE), which is hydrolyzed product of Baicalin (BA). on atopic dermatitis (AD). AD was induced in NC/Nga mice by DPE treatment BE hydrogels treatment reduced the levels of skin severity scores. BE hydrogels treatment also decreased inflammatory cytokines such as TNF-alpha, IL-6, and its level in the serum. BE hydrogels treatment elevated IFN-gamma level in the spleenocyte culture supernatant. Cell numbers in the skin positive to CD3+/CD69+, CCR3+, CD11b+/Gr-1+, B220+/IgE+ all of which were up-regulated in AD-induced mice were decreased and returned to normal levels. Histological examination showed that infiltration levels of immune cells in the skin of AD-induced NC/Nga mice were much improved by BE hydrogels treatment These results thus suggest that BE can regulate molecular mediators and immune cells that are functionally associated with atopic dermatitis induced in NC/Nga mice, and may play an important role in recovering AD symptoms. (C) 2010 Elsevier B.V. All rights reserved.
引用
收藏
页码:1142 / 1148
页数:7
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