The inhibitory effect of EGCG on high glucose-induced up-regulation of the expression of vascular cell adhesion molecule 1 (VCAM-1) was measured using enzyme-linked immunosorbent, RT-PCR, immunoblotting and cell adhesion assays. The effect of EGCG on high glucose-induced nuclear factor-kappa B (NF-¦ÊB) activation was investigated by immunoblotting, immunofluorescence and electrophoretic mobility shift assays.
High glucose increased VCAM-1 expression and enhanced the adhesion of monocytes to HUVECs. Pretreatment with EGCG in a concentration-dependent manner (1.0-50 ¦ÌM) significantly attenuated these effects. High glucose (25 mM)-mediated vascular inflammation was blocked by PKC pseudosubstrate (PKC inhibitor 19-31) or the NF-¦ÊB inhibitor pyrrolidine dithiocarbamate (PDTC). Stimulation with high glucose increased the NF-¦ÊB translocation from the cytoplasm to the nucleus, and increased I¦ÊB-¦Á phosphorylation, decreased its expression, and in the presence of EGCG, the effect of high glucose on NF-¦ÊB and I¦ÊB-¦Á were blocked.
EGCG suppresses high glucose-induced vascular inflammatory process via the inhibition of PKC and NF-¦ÊB activation in HUVECs, suggesting that EGCG may be a potential candidate for the treatment and prevention of diabetic vascular complications.