Epigallocatechin-3-gallate attenuates lipopolysaccharide-induced inflammation in human retinal endothelial cells
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1Hangzhou Vocational & Technical College, Hangzhou 310018, Zhejiang Province, China;
2Department of Ophthalmology, the First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, Zhejiang Province, China;
3State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, the First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, Zhejiang Province, China

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Supported by Public Technology Application Research Grant of Zhejiang Province (No.2011C33029); Natural Science Foundation of Zhejiang Province, China (No.LY13B020002)
Conflicts of Interest: Zhang HY, None; Wang JY, None; Yao HP, None.

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    Abstract:

    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: HRECs pre-treated with EGCG (0-100 μmol/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 LPS-stimulated 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 anti-inflammatory intervention.

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Hui-Yan Zhang, Jian-Yong Wang, Hang-Ping Yao. Epigallocatechin-3-gallate attenuates lipopolysaccharide-induced inflammation in human retinal endothelial cells. Int J Ophthalmol, 2014,7(3):408-412

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Publication History
  • Received:December 11,2013
  • Revised:March 05,2014
  • Adopted:March 05,2014
  • Online: June 24,2014
  • Published: