PMID- 17880982
OWN - NLM
STAT- MEDLINE
DCOM- 20080319
LR  - 20131121
IS  - 1879-1484 (Electronic)
IS  - 0021-9150 (Linking)
VI  - 197
IP  - 1
DP  - 2008 Mar
TI  - Comparative effects of quercetin and its predominant human metabolites on 
      adhesion molecule expression in activated human vascular endothelial cells.
PG  - 50-6
AB  - Adhesion of circulating monocytes to vascular endothelial cells, a critical step 
      in both inflammation and atherosclerosis, is mediated by cross-linkage of 
      adhesion molecules expressed on the surface of both cell types. Dietary 
      flavonoids have been shown to have anti-inflammatory properties, decreasing the 
      expression of cell adhesion molecules, such as vascular cell adhesion molecule-1 
      (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) on endothelial cells. 
      However, flavonoids are efficiently metabolised during absorption and the forms 
      reaching the systemic circulation are glucuronidated, sulphated and methylated. 
      Most previous in vitro studies of the effects of flavonoids have used the parent 
      compounds at concentrations far higher than those physiologically achievable. We 
      investigated the ability of quercetin and its human metabolites, at physiological 
      concentrations (2 micromol/L and 10 micromol/L), to attenuate the 
      inflammation-induced upregulated expression of VCAM-1, ICAM-1 and of the 
      chemokine, monocyte chemoattractant protein-1 (MCP-1), in human umbilical vein 
      endothelial cells (HUVECs), at the protein and transcript levels. Quercetin 
      treatment reduced the inflammation-induced over-expression of VCAM-1 and ICAM-1 
      (protein and transcript) in HUVECs. Quercetin also inhibited MCP-1 gene 
      expression. However, quercetin 3'-sulfate, quercetin 3-glucuronide and 
      3'-methylquercetin 3-glucuronide (isorhamnetin 3-glucuronide) generally exhibited 
      either a reduced ability to inhibit the expression of these molecules compared 
      with the parent aglycone or had no effect. However, all three metabolites 
      inhibited VCAM-1 cell surface expression at 2 micromol/L. These results indicate 
      that both quercetin and its metabolites, at physiological concentrations, can 
      inhibit the expression of key molecules involved in monocyte recruitment during 
      the early stages of atherosclerosis.
FAU - Tribolo, Sandra
AU  - Tribolo S
AD  - Phytochemicals and Health Programme, Institute of Food Research, Norwich Research 
      Park, Norwich NR4 7UA, UK.
FAU - Lodi, Federica
AU  - Lodi F
FAU - Connor, Carol
AU  - Connor C
FAU - Suri, Sunita
AU  - Suri S
FAU - Wilson, Vincent G
AU  - Wilson VG
FAU - Taylor, Moira A
AU  - Taylor MA
FAU - Needs, Paul W
AU  - Needs PW
FAU - Kroon, Paul A
AU  - Kroon PA
FAU - Hughes, David A
AU  - Hughes DA
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20070918
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 9IKM0I5T1E (Quercetin)
SB  - IM
MH  - Atherosclerosis/*drug therapy/immunology/pathology
MH  - Cell Adhesion/immunology
MH  - Cell Movement/immunology
MH  - Cell Survival
MH  - Cells, Cultured
MH  - Chemokine CCL2/genetics
MH  - Endothelial Cells/*drug effects/pathology/physiology
MH  - Gene Expression/drug effects
MH  - Humans
MH  - Intercellular Adhesion Molecule-1/*genetics/metabolism
MH  - Monocytes/pathology
MH  - Quercetin/*analogs & derivatives/*pharmacology
MH  - Umbilical Veins/cytology
MH  - Vascular Cell Adhesion Molecule-1/*genetics/metabolism
EDAT- 2007/09/21 09:00
MHDA- 2008/03/20 09:00
CRDT- 2007/09/21 09:00
PHST- 2007/06/01 00:00 [received]
PHST- 2007/07/27 00:00 [revised]
PHST- 2007/07/31 00:00 [accepted]
PHST- 2007/09/21 09:00 [pubmed]
PHST- 2008/03/20 09:00 [medline]
PHST- 2007/09/21 09:00 [entrez]
AID - S0021-9150(07)00483-2 [pii]
AID - 10.1016/j.atherosclerosis.2007.07.040 [doi]
PST - ppublish
SO  - Atherosclerosis. 2008 Mar;197(1):50-6. doi: 
      10.1016/j.atherosclerosis.2007.07.040. Epub 2007 Sep 18.