Suppr超能文献

(-)-表没食子儿茶素没食子酸酯和(- -)-表没食子儿茶素对HCT116结肠癌细胞增殖抑制活性的比较研究

Comparative examination of anti-proliferative activities of (-)-epigallocatechin gallate and (--)-epigallocatechin against HCT116 colorectal carcinoma cells.

作者信息

Inaba Hiroyuki, Nagaoka Yasuo, Kushima Yukihiro, Kumagai Ayako, Matsumoto Yoshinori, Sakaguchi Minoru, Baba Kimiye, Uesato Shinichi

机构信息

Department of Life Science and Biotechnology, Faculty of Chemistry, Material and Bioengineering, Kansai University, Suita, Osaka 564-8680, Japan.

出版信息

Biol Pharm Bull. 2008 Jan;31(1):79-84. doi: 10.1248/bpb.31.79.

Abstract

We compared anti-proliferative activities of (-)-epigallocatechin gallate (EGCG) and (-)-epigallocatechin (EGC) against HCT116 colorectal carcinoma cells. These catechins inhibited cell growth to nearly the same extent at low cell confluency in plates. However, their inhibitory effect grew weaker as cell confluence increased, and this tendency was more conspicuous for EGC than for EGCG. Both EGCG and EGC activated the phosphorylation of the major MAPKs, ERK, JNK, and p38, in the HCT116 cells as in many other established human cancer cells though to different extents. Cell cycle analyses, DNA fragmentation assays, and TUNEL assays as well as Western blot assays suggested that these catechins inhibited cell growth through mitogen-activated protein kinase (MAPK)-mediated apoptosis rather than cell cycle regulation.

摘要

我们比较了(-)-表没食子儿茶素没食子酸酯(EGCG)和(-)-表没食子儿茶素(EGC)对HCT116结肠癌细胞的抗增殖活性。在平板中细胞汇合度较低时,这些儿茶素对细胞生长的抑制程度几乎相同。然而,随着细胞汇合度增加,它们的抑制作用减弱,并且这种趋势在EGC中比在EGCG中更明显。与许多其他已建立的人类癌细胞一样,EGCG和EGC均能在不同程度上激活HCT116细胞中主要丝裂原活化蛋白激酶(MAPK)即细胞外调节蛋白激酶(ERK)、应激活化蛋白激酶(JNK)和p38的磷酸化。细胞周期分析、DNA片段化检测、末端脱氧核苷酸转移酶介导的缺口末端标记(TUNEL)检测以及蛋白质免疫印迹分析表明,这些儿茶素通过丝裂原活化蛋白激酶(MAPK)介导的凋亡而非细胞周期调节来抑制细胞生长。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验