Pon V Anandh Babu1, Hongwei Si, Dongmin Liu. 1. Department of Human Nutrition, Foods and Exercise, College of Agriculture and Life Sciences, Virginia Tech, Blacksburg, VA, USA.
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. 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. CONCLUSION: EGCG may have a direct protective effect against vascular inflammation in diabetes.
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-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-EGCGmice. 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-EGCGmice. CONCLUSION:EGCG may have a direct protective effect against vascular inflammation in diabetes.
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