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茶化合物通过抗氧化活性抑制培养的肝癌细胞的黏附和侵袭。

Suppression of adhesion and invasion of hepatoma cells in culture by tea compounds through antioxidative activity.

作者信息

Zhang G, Miura Y, Yagasaki K

机构信息

Department of Applied Biological Science, Tokyo Noko University, Saiwaicho 3-5-8, Fuchu, Tokyo 183-8509, Japan.

出版信息

Cancer Lett. 2000 Oct 31;159(2):169-73. doi: 10.1016/s0304-3835(00)00545-0.

DOI:10.1016/s0304-3835(00)00545-0
PMID:10996728
Abstract

To determine the actions of tea components on the invasion of a rat ascites hepatoma cell line of AH109A and to understand their modes of action, the cancer cells were co-cultured with a rat mesentery-derived mesothelial cell monolayer in the presence of tea components. The synergistic effects of (-)-epicatechin (EC) with (-)-epigallocatechin gallate (EGCG) on AH109A invasion were demonstrated. Further study showed that 10 microM of EGCG or theaflavins, or 2.5 microM of ethylenediaminetetra-acetic (EDTA) entirely abolished the increase in AH109A adhesion and invasion stimulated by reactive oxygen species (ROS) from the hypoxanthine-xanthine oxidase system. Our results suggest that (.)OH(-)- and other ROS-scavenging activity of EGCG and theaflavins may be responsible for the inhibition of (.)OH(-)- and related ROS-potentiated AH109A adhesion and invasion to the cultured rat mesothelial cell monolayer.

摘要

为了确定茶成分对大鼠腹水肝癌细胞系AH109A侵袭的作用,并了解其作用方式,将癌细胞与大鼠肠系膜来源的间皮细胞单层在茶成分存在的情况下进行共培养。结果表明,(-)-表儿茶素(EC)与(-)-表没食子儿茶素没食子酸酯(EGCG)对AH109A侵袭具有协同作用。进一步研究表明,10微摩尔的EGCG或茶黄素,或2.5微摩尔的乙二胺四乙酸(EDTA)完全消除了次黄嘌呤-黄嘌呤氧化酶系统产生的活性氧(ROS)刺激的AH109A黏附和侵袭的增加。我们的结果表明,EGCG和茶黄素的(·)OH-及其他ROS清除活性可能是抑制(·)OH-及相关ROS增强的AH109A对培养的大鼠间皮细胞单层的黏附和侵袭的原因。

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