Sulforaphane inhibits the Th2 immune response in ovalbumin-induced asthmaopen access
- Authors
- Park, Jun Ho; Kim, Jong Won; Lee, Chang-Min; Kim, Yeong Dae; Chung, Sung Woon; Jung, In Duk; Noh, Kyung Tae; Park, Jin Wook; Heo, Deok Rim; Shin, Yong Kyoo; Seo, Jong Keun; Park, Yeong-Min
- Issue Date
- May-2012
- Publisher
- KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY
- Keywords
- Asthma; GATA-3; SOCS3; Sulforaphane; Th1/Th2 balance
- Citation
- BMB REPORTS, v.45, no.5, pp 311 - 316
- Pages
- 6
- Journal Title
- BMB REPORTS
- Volume
- 45
- Number
- 5
- Start Page
- 311
- End Page
- 316
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/20312
- DOI
- 10.5483/BMBRep.2012.45.5.311
- ISSN
- 1976-6696
1976-670X
- Abstract
- 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]
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