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Epigallocatechin gallate reduces vascular inflammation in db/db mice possibly through an NF ‐κ B ‐mediated mechanism
Author(s) -
Babu Pon V. Anandh,
Si Hongwei,
Liu Dongmin
Publication year - 2012
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201200040
Subject(s) - inflammation , chemokine , chemistry , pathogenesis , endocrinology , medicine , diabetes mellitus , epigallocatechin gallate , endothelium , pharmacology , biochemistry , antioxidant , polyphenol
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. 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 ‐κ B ) regulated transcriptional activity in EC s. Six‐week‐old diabetic db/db mice were fed a diet containing 0% or 0.1% EGCG for 8 weeks. EC s were isolated from aortic vessels of db/db , db/db ‐ EGCG , and control db /+ mice. EGCG supplementation greatly suppressed diabetes‐increased monocytes adhesion to EC s, which is associated with reduced circulating levels of chemokines, and reduced secretions of chemokines and adhesion molecules by aortic EC s from db/db ‐ EGCG mice. EGCG treatment reduced nuclear translocation of NF ‐κ B p65 in aortic vessels, decreased blood pressure and serum concentrations of cholesterol and triglycerides in db/db ‐ EGCG mice. Conclusion EGCG may have a direct protective effect against vascular inflammation in diabetes.