Quercetin-3-O-β-D-Glucuronide Suppresses Lipopolysaccharide-Induced JNK and ERK Phosphorylation in LPS-Challenged RAW264.7 Cells.
10.4062/biomolther.2016.026
- Author:
Jin Young PARK
1
;
Man Sup LIM
;
Song In KIM
;
Hee Jae LEE
;
Sung Soo KIM
;
Yong Soo KWON
;
Wanjoo CHUN
Author Information
1. Department of Pharmacology, College of Medicine, Chuncheon 24341, Republic of Korea. wchun@kangwon.ac.kr
- Publication Type:Original Article
- Keywords:
Quercetin-3-O-β-D-glucuronide;
Quercetin;
RAW264.7 cells;
Lipopolysaccharide;
JNK;
ERK
- MeSH:
Dinoprostone;
Macrophages;
Nitric Oxide;
Phosphorylation*;
Quercetin
- From:Biomolecules & Therapeutics
2016;24(6):610-615
- CountryRepublic of Korea
- Language:English
-
Abstract:
Quercetin, a flavonol, has been reported to exhibit a wide range of biological properties including anti-oxidant and anti-inflammatory activities. However, pharmacological properties of quercetin-3-O-β-D-glucuronide (QG), a glycoside derivative of quercetin, have not been extensively examined. The objective of this study is to elucidate the anti-inflammatory property and underlying mechanism of QG in lipopolysaccharide (LPS)-challenged RAW264.7 macrophage cells in comparison with quercetin. QG significantly suppressed LPS-induced extracellular secretion of pro-inflammatory mediators such as nitric oxide (NO) and PGE2, and pro-inflammatory protein expressions of iNOS and COX-2. To elucidate the underlying mechanism of the anti-inflammatory property of QG, involvement of MAPK signaling pathways was examined. QG significantly attenuated LPS-induced activation of JNK and ERK in concentration-dependent manners with a negligible effect on p38. In conclusion, the present study demonstrates QG exerts anti-inflammatory activity through the suppression of JNK and ERK signaling pathways in LPS-challenged RAW264.7 macrophage cells.
