Sulforaphane inhibits the Th2 immune response in ovalbumin-induced asthma

被引:33
作者
Park, Jun Ho [2 ]
Kim, Jong Won [2 ]
Lee, Chang-Min [1 ]
Kim, Yeong Dae [3 ]
Chung, Sung Woon [3 ]
Jung, In Duk [1 ]
Noh, Kyung Tae [1 ]
Park, Jin Wook [1 ]
Heo, Deok Rim [1 ]
Shin, Yong Kyoo [4 ]
Seo, Jong Keun [5 ]
Park, Yeong-Min [1 ]
机构
[1] Pusan Natl Univ, Sch Med, Dept Microbiol & Immunol, Yangsan 626770, South Korea
[2] Busan Med Ctr, Dept Thorac & Cardiovasc Surg, Pusan 611672, South Korea
[3] Pusan Natl Univ, Sch Med, Dept Thorac & Cardiovasc Surg, Pusan 602739, South Korea
[4] Chung Ang Univ, Coll Med, Dept Pharmacol, Seoul 156756, South Korea
[5] Inje Univ, Coll Med, Busan Paik Hosp, Dept Dermatol, Pusan 614735, South Korea
关键词
Asthma; GATA-3; SOCS3; Sulforaphane; Th1/Th2; balance; T-CELLS; AIRWAY INFLAMMATION; DENDRITIC CELLS; KAPPA-B; EOSINOPHILS; APOPTOSIS; PROTEIN; MICE;
D O I
10.5483/BMBRep.2012.45.5.311
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Sulforaphane (1-isothiocyanato-4-(methylsulfinyl)-butane), belonging to a family of natural compounds that are abundant in broccoli, has received significant therapeutic interest in recent years. However, the molecular basis of its effects remains to be elucidated. In this study, we attempt to determine whether sulforaphane regulates the inflammatory response in an ovalbumin (OVA)-induced murine asthma model. Mice were sensitized with OVA, treated with sulforaphane, and then challenged with OVA. Sulforaphane administration significantly alleviated the OVA-induced airway hyperresponsiveness to inhaled methacholine. Additionally, sulforaphane suppressed the increase in the levels of SOCS-3 and GATA-3 and IL-4 expression in the OVA-challenged mice. Collectively, our results demonstrate that sulforaphane regulates Th2 immune responses. This sutdy provides novel insights into the regulatory role of sulforaphane in allergen-induced Th2 inflammation and airway responses, which indicates its therapeutic potential for asthma and other allergic diseases. [BMB Reports 2012; 45(5): 311-316]
引用
收藏
页码:311 / 316
页数:6
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