title: EGCG attenuates high glucose-induced endothelial cell inflammation by suppression of PKC and NF-κB signaling in human umbilical vein endothelial cells.
abstract: OBJECTIVE
  Vascular inflammation is a key factor in the pathogenesis of diabetes-related vascular complications. Our previous study showed that (-)-epigallocatechin-3-gallate (EGCG) inhibits high glucose-induced vascular smooth muscle cell proliferation, thus it may have beneficial effects in diabetes and its complications. However, the effect of EGCG on inflammation in diabetes is not known. In the present study, we investigated whether EGCG suppresses the vascular inflammation induced by high glucose in human umbilical vein endothelial cells (HUVECs).
  
  
  METHODS
  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-κB) activation was investigated by immunoblotting, immunofluorescence and electrophoretic mobility shift assays.
  
  
  RESULTS
  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 μM) significantly attenuated these effects. High glucose (25 mM)-mediated vascular inflammation was blocked by PKC pseudosubstrate (PKC inhibitor 19-31) or the NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC). Stimulation with high glucose increased the NF-κB translocation from the cytoplasm to the nucleus, and increased IκB-α phosphorylation, decreased its expression, and in the presence of EGCG, the effect of high glucose on NF-κB and IκB-α were blocked.
  
  
  CONCLUSIONS
  EGCG suppresses high glucose-induced vascular inflammatory process via the inhibition of PKC and NF-κB activation in HUVECs, suggesting that EGCG may be a potential candidate for the treatment and prevention of diabetic vascular complications.
authors: Department of Nutrition, Daping Hospital, The Third Military Medical University, Chongqing, PR China.
authors: Jian
authors: J
authors: Yang
authors: Yu
authors: Y
authors: Han
authors: Caiyu
authors: C
authors: Chen
authors: Hailan
authors: H
authors: Sun
authors: Duofen
authors: D
authors: He
authors: Jing
authors: J
authors: Guo
authors: Baoquan
authors: B
authors: Jiang
authors: Lin
authors: L
authors: Zhou
authors: Chunyu
authors: C
authors: Zeng
mesh_terms: D001786:Blood Glucose; D002392:Catechin / Q000031:analogs & derivatives* / Q000737:chemistry / Q000494:pharmacology; D048909:Diabetes Complications / Q000378:metabolism*; D024202:Electrophoretic Mobility Shift Assay; D004797:Enzyme-Linked Immunosorbent Assay; D005455:Fluorescent Antibody Technique; D061307:Human Umbilical Vein Endothelial Cells; D006801:Humans; D015151:Immunoblotting; D007249:Inflammation / Q000188:drug therapy* / Q000209:etiology; D015394:Molecular Structure; D016328:NF-kappa B / Q000378:metabolism*; D011493:Protein Kinase C / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000187:drug effects*; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism*
chemical_list: D001786:Blood Glucose; D016328:NF-kappa B; D019010:Vascular Cell Adhesion Molecule-1; D002392:Catechin; C045651:epigallocatechin gallate; D011493:Protein Kinase C