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AIM:To investigate the mechanism underlying the anti-inflammatory effects of epigallocatechin-3-gallate(EGCG)in lipopolysaccharide(LPS)-stimulated human retinal endothelial cells(HRECs).METHODS:HRECspre-treatedwithEGCG(0-100μmol/L)were stimulated with LPS(250 ng/mL).Levels of tumor necrosis factor alpha(TNF-α),vascular endothelial growth factor(VEGF),monocyte chemotactic protein-1(MCP-1)and nitric oxide(NO)in the supernatants were determined by enzyme-linked immunosorbent assay(ELISA)and Griess assay.The protein expression of phosphorylated extracellular signal-regulated kinase(ERK)1/2 and p38 mitogen-activated protein kinases(p38)were determined by Western blot analysis.RESULTS:EGCG pre-treatment significantly inhibited the secretion of TNF-α,VEGF,MCP-1 and NO in LPSstimulated HRECs.Moreover,EGCG effectively attenuated LPS-induced activation and phosphorylation of ERK1/2 and p38 in HRECs in a dose-dependent manner.CONCLUSION:EGCG exhibited inhibitory effects on LPS-induced pro-inflammatory cytokines production by modulating ERK1/2 and p38 pathways in HRECs,suggesting EGCG as a potential candidate for antiinflammatory intervention.
AIM: To investigate the mechanism underlying the anti-inflammatory effects of epigallocatechin-3-gallate (LPS) -stimulated human retinal endothelial cells (HRECs). METHODS: HRECs pre-treated with EGCG (0-100 μmol / L) with LPS (250 ng / mL) .Levels of tumor necrosis factor alpha (TNF-α), vascular endothelial growth factor (VEGF), monocyte chemotactic protein- 1 (MCP-1) and nitric oxide (NO) in the supernatants were determined by enzyme-linked immunosorbent assay (ELISA) and Griess assay. The protein expression of phosphorylated extracellular signal-regulated kinase (ERK) 1/2 and p38 mitogen-activated protein kinases (p38) were determined by Western blot analysis.RESULTS: EGCG pre -treatment significantly inhibited the secretion of TNF-α, VEGF, MCP-1 and NO in LPSstimulated HRECs. Moreover, EGCG substantially attenuated LPS-induced activation and phosphorylation of ERK1 / 2 and p38 in HRECs in a dose-dependent manner. CONCLUSION: EGCG exhibited inhibitory effects on LPS-induced pro-infl ammatory cytokines production by modulating ERK1 / 2 and p38 pathways in HRECs, suggesting EGCG as a potential candidate for antiinflammatory intervention.