| Cellular Physiology and Biochemistry | |
| Green Tea Polyphenol Epigallocatechin-3-Gallate Inhibits TNF-a-Induced Production of Monocyte Chemoattractant Protein-1 in Human Umbilical Vein Endothelial Cells | |
| 关键词: Green tea; Epigallocatechin-3-gallate; Monocyte chemoattractant protein-1; Human umbilical vein endothelial cells; | |
| DOI : 10.1159/000358702 | |
| 学科分类:分子生物学,细胞生物学和基因 | |
| 来源: S Karger AG | |
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【 摘 要 】
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.
【 授权许可】
CC BY-NC-ND
【 预 览 】
| Files | Size | Format | View |
|---|---|---|---|
| RO201904037051225ZK.pdf | 1648KB |
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