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Epigallocatechin gallate reduces vascular inflammation in db/db mice possibly through an NF-κB-mediated mechanism.

Authors :
Babu PV
Si H
Liu D
Source :
Molecular nutrition & food research [Mol Nutr Food Res] 2012 Sep; Vol. 56 (9), pp. 1424-32. Date of Electronic Publication: 2012 Jul 02.
Publication Year :
2012

Abstract

Scope: Hyperglycemia-induced vascular inflammation resulting in the adhesion of monocytes to endothelium is a key event in the pathogenesis of atherosclerosis in diabetes. We investigated whether epigallocatechin gallate (EGCG), a major catechin found in green tea, reduces vascular inflammation in diabetes.<br />Methods and Results: Human aortic endothelial cells (HAEC) were pretreated with green tea catechins before the addition of high glucose (25 mM) for 72 h. EGCG at physiologically achievable concentration (1 μM) significantly inhibited high glucose induced adhesion of monocytes to HAEC both in static and under flow conditions. EGCG also reduced nuclear factor κB (NF-κB) regulated transcriptional activity in ECs. Six-week-old diabetic db/db mice were fed a diet containing 0% or 0.1% EGCG for 8 weeks. ECs were isolated from aortic vessels of db/db, db/db-EGCG, and control db/+ mice. EGCG supplementation greatly suppressed diabetes-increased monocytes adhesion to ECs, which is associated with reduced circulating levels of chemokines, and reduced secretions of chemokines and adhesion molecules by aortic ECs from db/db-EGCG mice. EGCG treatment reduced nuclear translocation of NF-κB p65 in aortic vessels, decreased blood pressure and serum concentrations of cholesterol and triglycerides in db/db-EGCG mice.<br />Conclusion: EGCG may have a direct protective effect against vascular inflammation in diabetes.<br /> (© 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Details

Language :
English
ISSN :
1613-4133
Volume :
56
Issue :
9
Database :
MEDLINE
Journal :
Molecular nutrition & food research
Publication Type :
Academic Journal
Accession number :
22753231
Full Text :
https://doi.org/10.1002/mnfr.201200040