6-Acetonyl-5,6-dihydrosanguinarine (ADS) from Chelidonium majus L. triggers proinflammatory cytokine production via ROS-JNK/ERK-NF kappa B signaling pathway
- Authors
- Kim, Dong Hyeok; Lee, Ji Hye; Park, Soojong; Oh, Sang-seok; Kim, Suk; Kim, Dae Wook; Park, Ki Hun; Kim, Kwang Dong
- Issue Date
- Aug-2013
- Publisher
- PERGAMON-ELSEVIER SCIENCE LTD
- Keywords
- Chelidonium majus; 6-Acetonyl-5,6-dihydrosanguinarine; Inflammatory cytokine; NF kappa B; ROS; MAPK
- Citation
- FOOD AND CHEMICAL TOXICOLOGY, v.58, pp.273 - 279
- Indexed
- SCIE
SCOPUS
- Journal Title
- FOOD AND CHEMICAL TOXICOLOGY
- Volume
- 58
- Start Page
- 273
- End Page
- 279
- URI
- https://scholarworks.bwise.kr/gnu/handle/sw.gnu/20565
- DOI
- 10.1016/j.fct.2013.04.051
- ISSN
- 0278-6915
- Abstract
- Chelidonium majus L is an herbal plant that is commonly used in Western phytotherapy and traditional Chinese medicine for diuretic, antitussive, eye-regenerative, anti-osteoporotic, and radioprotective purposes. In this study, we purified 6-acetonyl-5,6-dihydrosanguinarine (ADS) from C majus and investigated its immune-stimulatory effect. We found that ADS has the potential to induce the inflammatory cytokines TNF-alpha, IL-6, and IL-8 in macrophages and dendritic cells (DCs), that NF kappa B activation is a critical mediator of ADS-induced cytokine production, and that the activation of NF kappa B was dependent on reactive oxygen species (ROS). ADS induced phosphorylation of ERK and JNK, which was also associated with NF kappa B activation; phosphoiylarion and cytokine production were inhibited by ROS scavenger and by specific MAPK inhibitors. Taken together, the results suggest that ADS from C majus, as a positive immune modulator, induces inflammatory cytokines that might improve immunity, via the ROS-ERK/JNK-NF kappa B pathway. (C) 2013 Elsevier Ltd. All rights reserved.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - 수의과대학 > Department of Veterinary Medicine > Journal Articles
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.