Biomol Ther.  2016 Nov;24(6):610-615. 10.4062/biomolther.2016.026.

Quercetin-3-O-β-D-Glucuronide Suppresses Lipopolysaccharide-Induced JNK and ERK Phosphorylation in LPS-Challenged RAW264.7 Cells

• Park JY
• Lim MS
• Kim SI
• Lee HJ
• Kim SS
• Kwon YS
• Chun W

• KMID: 2374615
• DOI: http://doi.org/10.4062/biomolther.2016.026

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.

Keyword

Quercetin-3-O-β-D-glucuronide; Quercetin; RAW264.7 cells; Lipopolysaccharide; JNK; ERK

MeSH Terms

Dinoprostone
Macrophages
Nitric Oxide
Phosphorylation*
Quercetin
Dinoprostone
Nitric Oxide
Quercetin