The essential role of JNK1 for the development of atopic dermatitis and the preventive effect of JNK1 inhibiting phytochemicals luteolin and licochalcone A

Atopic dermatitis;JNK1;luteolin;licochalcone A;630

농업생명과학대학 농생명공학부 ;

University:서울대학교 대학원

关键词: Atopic dermatitis;    JNK1;    luteolin;    licochalcone A;    630;   

Others  :  http://s-space.snu.ac.kr/bitstream/10371/125806/1/000000012580.pdf

美国|英语

来源: Seoul National University Open Repository

【 摘 要 】

Atopic dermatitis (AD) is a common allergic disease, imposing large social and economic burdens worldwide. AD is characterized by eczematous skin lesions and immunoglobulin E (IgE) hypersecretion. I investigated the role of c-Jun N-terminal kinase 1 (JNK1) and the effect of JNK1-inhibiting phytochemicals on the development of AD in mice. The vitamin D3 analogue MC903 was used to induce AD in wild-type (WT) and JNK1−/− mice. The symptoms of AD were less severe in JNK1−/− mice compared to WT mice. JNK1−/− mice showed less ear thickening and infiltration of eosinophils and mast cells in AD-like lesions than did WT mice when treated with MC903. MC903-treated JNK1−/− mice also showed lower levels of serum IgE, which was significantly elevated in MC903-treated WT mice. Splenocytes isolated from MC903-treated WT and JNK1−/− mice were stimulated with anti-CD3 and anti-CD28 monoclonal antibodies. Splenocytes from JNK1−/− mice produced lower levels of T-helper (Th)2 cytokines (interleukin-4 and -13) and transcription factor GATA-binding protein 3, and produced increased levels of the Th1 cytokines interferon-g and transcription factor T-box expressed in T cells. The JNK1-inhibiting phytochemicals luteolin and licochalcone A prevented MC903-induced ear thickening and the increase in serum IgE, suggesting that these compounds could prevent the development of AD. Our results indicate that JNK1 plays an important role in the pathogenesis of AD and may be a useful target for food-based therapies to prevent AD.