Wang Ze-Mu, Gao Wei, Wang Hao, Zhao Di, Nie Zhen-Lin, Shi Jian-Quan, Zhao Shan, Lu Xiang, Wang Lian-Sheng, Yang Zhi-Jian
Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Cell Physiol Biochem. 2014;33(5):1349-58. doi: 10.1159/000358702. Epub 2014 May 5.
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-α (TNF-α)-induced production of monocyte chemoattractant protein-1 (MCP-1) in human umbilical vein endothelial cells (HUVECs) and investigated the underlying molecular mechanisms.
The inhibitory effect of EGCG on TNF-α-induced expression of MCP-1 was measured using ELISA and RT-qPCR. The effect of EGCG on TNF-α-induced nuclear factor-kappa B (NF-κB) activation was investigated by western blot and luciferase assays. Monocyte adhesion assay was detected by microscope.
EGCG significantly suppressed the TNF-α-induced protein and mRNA expression of MCP-1. Investigation of the mechanism suggested that EGCG suppressed the TNF-α-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.
EGCG suppresses TNF-α-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.
表没食子儿茶素-3-没食子酸酯(EGCG)是绿茶中发现的一种主要儿茶素,具有多种药理特性,最近作为心血管疾病(CVD)的一种潜在饮食干预措施受到关注。本研究旨在验证EGCG能够抑制肿瘤坏死因子-α(TNF-α)诱导人脐静脉内皮细胞(HUVECs)产生单核细胞趋化蛋白-1(MCP-1)这一假说,并探究其潜在的分子机制。
采用酶联免疫吸附测定(ELISA)和逆转录定量聚合酶链反应(RT-qPCR)检测EGCG对TNF-α诱导的MCP-1表达的抑制作用。通过蛋白质免疫印迹法和荧光素酶测定法研究EGCG对TNF-α诱导的核因子-κB(NF-κB)激活的影响。通过显微镜检测单核细胞黏附试验。
EGCG显著抑制TNF-α诱导的MCP-1蛋白和mRNA表达。机制研究表明,EGCG抑制TNF-α介导的NF-κB激活。此外,67-kD层粘连蛋白受体(67LR)参与了EGCG介导的对MCP-1生成的抑制作用。此外,EGCG强烈抑制单核细胞对活化的HUVECs的黏附。
EGCG抑制TNF-α诱导的HUVECs中MCP-1的表达。这种作用由67LR介导,并且是通过抑制NF-κB激活实现的。我们的结果表明,EGCG可能是一种预防和治疗CVD的潜在药物。