- Title
- Columbianadin suppresses lipopolysaccharide (LPS)-induced inflammation and apoptosis through the NOD1 pathway
- Creator
- Zhang, Chao; Chen-Yu Hsu, Alan; Wang, Fang; Pan, He; Gu, Yinuo; Zuo, Xu; Dong, Bing; Wang, Ziyan; Zheng, Jingtong; Lu, Junying; Zheng, Ruipeng
- Relation
- Molecules Vol. 24, Issue 3, p. 1-12
- Publisher Link
- http://dx.doi.org/10.3390/molecules24030549
- Publisher
- MDPI AG
- Resource Type
- journal article
- Date
- 2019
- Description
- Columbianadin (CBN) is one of the main bioactive constituents isolated from the root of Angelica pubescens. Although the anti-inflammatory activity of CBN has been reported, the underpinning mechanism of this remains unclear. In this study, we investigated the anti-inflammatory effect of CBN on lipopolysaccharide (LPS)-stimulated THP-1 cells and explored the possible underlying molecular mechanisms. The results showed that CBN suppressed LPS-mediated inflammatory response mainly through the inactivation of the NOD1 and NF- B p65 signaling pathways. Knockdown of NOD1 reduced the degree to which inflammatory cytokines decreased following CBN treatment, whereas forced expression of NOD1 and CBN treatment reduced NF- Bp65 activation and the secretion of inflammatory cytokines. Furthermore, CBN significantly reduced cellular apoptosis by inhibiting the NOD1 pathway. Collectively, our results indicate that CBN suppressed the LPS-mediated inflammatory response by inhibiting NOD1/NF- B activation. Furtherinvestigations are required to determine the mechanisms of action of CBN in the inhibition of NOD signaling: However, CBN may be employed as a therapeutic agent for multiple inflammatory diseases.
- Subject
- columbianadin; inflammation; NOD1; NF-B
- Identifier
- http://hdl.handle.net/1959.13/1455448
- Identifier
- uon:45089
- Identifier
- ISSN:1420-3049
- Rights
- This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. https://creativecommons.org/licenses/by/4.0/
- Language
- eng
- Full Text
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