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首页> 外文期刊>Biological & pharmaceutical bulletin >Comparative examination of anti-proliferative activities of (-)-epigallocatechin gallate and (-)-epigallocatechin against HCT116 colorectal carcinoma cells
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Comparative examination of anti-proliferative activities of (-)-epigallocatechin gallate and (-)-epigallocatechin against HCT116 colorectal carcinoma cells

机译:(-)-表没食子儿茶素没食子酸酯和(-)-表没食子儿茶素对HCT116结直肠癌细胞的抗增殖活性的比较检查

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摘要

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.
机译: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大肠癌细胞的抗增殖活性。这些儿茶素在平板中的低细胞融合度下将细胞生长抑制到几乎相同的程度。然而,随着细胞融合的增加,它们的抑制作用变得更弱,并且这种趋势对于EGC比对于EGCG更明显。尽管在不同程度上,EGCG和EGC都像许多其他已建立的人类癌细胞一样激活了HCT116细胞中主要MAPK,ERK,JNK和p38的磷酸化。细胞周期分析,DNA片段化分析和TUNEL分析以及Western blot分析表明,这些儿茶素通过有丝分裂原激活的蛋白激酶(MAPK)介导的凋亡而不是细胞周期调节来抑制细胞生长。

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