Document
Anti-inflammatory effects of a polyphenol, catechin-7,4'-o-digallate, from woodfordia uniflora by regulating nf-κb signaling pathway in mouse macrophages.
Identifier
DOI: 10.3390/pharmaceutics13030408
Source
Pharmaceutics. v. 13, 3, 408
Contributors
Seo, Ji Bin., Author
Yu, Jae Sik., Author
Lee, Seoyoung., Author
Lim, Jae Sung., Author
Choi, Jeong Uk., Author
Lee, Chang-Min., Author
Rashan, Luay., Author
Kim, Ki Hyun., Author
Cho, Young-Chang., Author
Country
Switzerland
Publisher
MDPI AG.
Gregorian
2021-03-01
Language
English
Subject
English abstract
Inflammation is a defense mechanism that protects the body from infections. However, chronic inflammation causes damage to body tissues. Thus, controlling inflammation and investigating anti-inflammatory mechanisms are keys to preventing and treating inflammatory diseases, such as sepsis and rheumatoid arthritis. In continuation with our work related to the discovery of bioactive natural products, a polyphenol, catechin-7,4'-O-digallate (CDG), was isolated from Woodfordia uniflora, which has been used as a sedative and remedy for skin infections in the Dhofar region of Oman. Thus far, no study has reported the anti-inflammatory compounds derived from W. uniflora and the mechanisms underlying their action. To investigate the effects of CDG on the regulation of inflammation, we measured the reduction in nitric oxide (NO) production following CDG treatment in immortalized mouse Kupffer cells (ImKCs). CDG treatment inhibited NO production through the downregulation of inducible nitric oxide synthase expression in lipopolysaccharide (LPS)-stimulated ImKCs. The anti-inflammatory effects of CDG were mediated via the inhibition of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, an important inflammatory- response-associated signaling pathway. Moreover, CDG treatment has regulated the expression of pro-inflammatory cytokines, such as IL-6 and IL-1β. These results suggested the antiinflammatory action of CDG in LPS-stimulated ImKCs.
ISSN
1999-4923
Resource URL
Category
Journal articles