PMID- 18489909
OWN - NLM
STAT- MEDLINE
DCOM- 20090408
LR  - 20161125
IS  - 1879-1484 (Electronic)
IS  - 0021-9150 (Linking)
VI  - 202
IP  - 2
DP  - 2009 Feb
TI  - Physiologically relevant metabolites of quercetin have no effect on adhesion 
      molecule or chemokine expression in human vascular smooth muscle cells.
PG  - 431-8
LID - 10.1016/j.atherosclerosis.2008.04.040 [doi]
AB  - Dietary flavonoids have been shown to have a number of anti-inflammatory 
      properties, including decreasing the expression of adhesion molecules. Flavonoids 
      however, are metabolised during absorption and the forms reaching the systemic 
      circulation are glucuronidated, sulfated and methylated. Most previous studies of 
      the effects of flavonoids have used the parent compounds rather than the 
      metabolites found in blood plasma and we have recently shown that metabolites of 
      quercetin can retain some of the anti-inflammatory properties of the parent 
      aglycone when used to treat human umbilical endothelial cells (HUVEC). Using both 
      physiologically achievable (2 microM) and supraphysiological (10 microM) 
      concentrations, we investigated the ability of quercetin and its predominant 
      human metabolites to attenuate the expression of vascular cell adhesion 
      molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1) and monocyte 
      chemoattractant protein-1 (MCP-1) in human umbilical artery smooth muscle cells 
      (HUASMC) activated by tumor necrosis factor-alpha (TNFalpha). Quercetin was able 
      to reduce TNFalpha-induced upregulation of VCAM-1, ICAM-1 and MCP-1 at both the 
      protein and transcript (mRNA) level in HUASMC. However the quercetin metabolites, 
      quercetin 3'-sulfate, quercetin 3-glucuronide and 3'-methylquercetin 
      3-glucuronide, had no effect on TNFalpha-induced up regulation of adhesion 
      molecule or chemokine expression, at either concentration tested. These data do 
      not support the notion that the vascular anti-inflammatory effects of quercetin 
      consumption are mediated through effects on smooth muscle cells.
FAU - Winterbone, Mark S
AU  - Winterbone MS
AD  - Phytochemicals and Health Programme, Institute of Food Research, Norwich Research 
      Park, Norwich, Norfolk, NR4 7UA, UK. mark.winterbone@bbsrc.ac.uk
FAU - Tribolo, Sandra
AU  - Tribolo S
FAU - Needs, Paul W
AU  - Needs PW
FAU - Kroon, Paul A
AU  - Kroon PA
FAU - Hughes, David A
AU  - Hughes DA
LA  - eng
GR  - Biotechnology and Biological Sciences Research Council/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20080501
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokines)
RN  - 0 (Flavonols)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 0 (quercetin 3'-sulfate)
RN  - 0 (quercetin 3-O-glucuronide)
RN  - 07X3IB4R4Z (3-methylquercetin)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 9IKM0I5T1E (Quercetin)
SB  - IM
MH  - Cell Division/drug effects/physiology
MH  - Cell Survival/drug effects/physiology
MH  - Cells, Cultured
MH  - Chemokine CCL2/*genetics
MH  - Chemokines/physiology
MH  - Flavonols/pharmacology
MH  - Gene Expression/drug effects/physiology
MH  - Humans
MH  - Intercellular Adhesion Molecule-1/*genetics
MH  - Muscle, Smooth, Vascular/*cytology
MH  - Myocytes, Smooth Muscle/cytology/*drug effects/immunology
MH  - Quercetin/*analogs & derivatives/pharmacology
MH  - RNA, Messenger/metabolism
MH  - Tumor Necrosis Factor-alpha/pharmacology
MH  - Umbilical Arteries/cytology
MH  - Vascular Cell Adhesion Molecule-1/*genetics
EDAT- 2008/05/21 09:00
MHDA- 2009/04/09 09:00
CRDT- 2008/05/21 09:00
PHST- 2008/04/04 00:00 [received]
PHST- 2008/04/04 00:00 [accepted]
PHST- 2008/05/21 09:00 [pubmed]
PHST- 2009/04/09 09:00 [medline]
PHST- 2008/05/21 09:00 [entrez]
AID - S0021-9150(08)00278-5 [pii]
AID - 10.1016/j.atherosclerosis.2008.04.040 [doi]
PST - ppublish
SO  - Atherosclerosis. 2009 Feb;202(2):431-8. doi: 
      10.1016/j.atherosclerosis.2008.04.040. Epub 2008 May 1.