Cellular Physiology and Biochemistry (May 2014)

Green Tea Polyphenol Epigallocatechin-3-Gallate Inhibits TNF-a-Induced Production of Monocyte Chemoattractant Protein-1 in Human Umbilical Vein Endothelial Cells

  • Ze-Mu Wang,
  • Wei Gao,
  • Hao Wang,
  • Di Zhao,
  • Zhen-Lin Nie,
  • Jian-Quan Shi,
  • Shan Zhao,
  • Xiang Lu,
  • Lian-Sheng Wang,
  • Zhi-Jian Yang

DOI
https://doi.org/10.1159/000358702
Journal volume & issue
Vol. 33, no. 5
pp. 1349 – 1358

Abstract

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Aims: Epigallocatechin-3-gallate (EGCG), a major catechin found in green tea, displays a variety of pharmacological properties and recently received attention as a prospective dietary intervention in cardiovascular diseases (CVD). This study was conducted to test the hypothesis that EGCG was able to inhibit tumor necrosis factor-a (TNF-a)-induced production of monocyte chemoattractant protein-1 (MCP-1) in human umbilical vein endothelial cells (HUVECs) and investigated the underlying molecular mechanisms. Methods: The inhibitory effect of EGCG on TNF-a-induced expression of MCP-1 was measured using ELISA and RT-qPCR. The effect of EGCG on TNF-a-induced nuclear factor-kappa B (NF-κB) activation was investigated by western blot and luciferase assays. Monocyte adhesion assay was detected by microscope. Results: EGCG significantly suppressed the TNF-a-induced protein and mRNA expression of MCP-1. Investigation of the mechanism suggested that EGCG suppressed the TNF-a-mediated NF-κB activation. In addition, the 67-kD laminin receptor (67LR) was involved in EGCG-mediated suppression of MCP-1 generation. Furthermore, EGCG potently inhibited monocyte adhesion to activated HUVECs. Conclusion: EGCG suppresses TNF-a-induced MCP-1 expression in HUVECs. This effect was mediated by 67LR and was via the inhibition of NF-κB activation. Our results demonstrated that EGCG might be a possible medicine for CVD prevention and treatment.

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