(‑)‑Epigallocatechin‑3‑Gallate Protects against Uric Acid‑Induced Endothelial Dysfunction in Human Umbilical Vein Endothelial Cells

Background: Hyperuricemia is recently reported to be associated with hypertension, metabolic syndrome, and vascular damage. (‑)‑Epigallocatechin gallate (EGCG) is a major polyphenol component of green tea involving in potent anti‑inflammatory and antioxidant effects. The study assessed the effect of EGCG on uric acid (UA)‑induced vascular damage. Materials and Methods: The cell viability and angiogenic formation of human umbilical vein endothelial cells (HUVECs) treated with UA and EGCG were determined by methylthiazol tetrazolium and tube formation assays, respectively. The expression level of inflammatory cytokine and vascular factor, including nuclear factor‑kappa B (NF‑κB), monocyte chemotactic protein‑1 (MCP‑1), intercellular adhesion molecule 1 (ICAM‑1), cycloxygenase‑2, tumor necrosis factor (TNF‑α), induced nitric oxide synthetase (iNOS), endothelin‑1 (ET‑1), and von Willebrand factor, were examined by real‑time quantitative reverse transcription polymerase chain reaction. The expression of P65 in HUVECs treated with UA in different time points or different concentrations was detected by Western blotting. Results: EGCG suppressed UA‑inducing HUVEC cells death. UA treatment of HUVEC significantly increases the expression of P65. EGCG significantly inhibited the UA‑induced mRNA expression of NF‑κB, MCP‑1, ICAM‑1, TNF‑α, iNOS, and ET‑1 in HUVECs. Functional analysis of angiogenic inhibition showed that pretreatment with EGCG improved the vascular tube formation. Conclusion: Our results suggested that UA‑induced inflammatory cytokine production and impaired endothelial cell function in HUVECs were attenuated by EGCG. These data indicated that EGCG has a therapeutic potential for UA‑mediated endothelial damage.