期刊
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
卷 33, 期 5, 页码 1349-1358出版社
KARGER
DOI: 10.1159/000358702
关键词
Green tea; Epigallocatechin-3-gallate; Monocyte chemoattractant protein-1; Human umbilical vein endothelial cells
资金
- National Natural Science Foundation of China [81270255, 30971254]
- Science and Technological Innovation Group of Jiangsu Higher Education Institution Qing-Lan Project [JX2161015030]
- Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
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-alpha)-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-alpha-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-kappa B) 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-alpha-mediated NF-kappa B 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-alpha-induced MCP-1 expression in HUVECs. This effect was mediated by 67LR and was via the inhibition of NF-kappa B activation. Our results demonstrated that EGCG might be a possible medicine for CVD prevention and treatment. Copyright (C) 2014 S. Karger AG, Basel
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