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当代肿瘤药物靶点

Editor-in-Chief

ISSN (Print): 1568-0096
ISSN (Online): 1873-5576

Research Article

表没食子儿茶素-3-没食子酸酯通过ROS介导的AKT / JNK和p53信号通路诱导HepG2细胞凋亡

卷 23, 期 6, 2023

发表于: 22 February, 2023

页: [447 - 460] 页: 14

弟呕挨: 10.2174/1568009622666220705101642

价格: $65

摘要

背景:肝癌是全世界癌症相关死亡的第三大原因。最近,一些研究报道表没食子儿茶素-3-没食子酸酯(EGCG)可能具有抗癌潜力。然而,EGCG 在 HepG2 细胞中诱导的细胞毒性的影响和推定机制仍然未知。基于此,本研究评估了EGCG对HepG2细胞的细胞毒性和抗癌机制的影响。 方法:通过细胞计数试剂盒8、JC-1线粒体膜电位检测、Annexin V-FITC细胞凋亡检测、细胞周期、细胞凋亡分析等方法研究EGCG对Hep-G2细胞凋亡的影响及其机制。步骤 TUNEL 细胞凋亡测定、半胱天冬酶 3 活性测定、半胱天冬酶 9 活性测定、活性氧物种测定和蛋白质印迹。 结果:EGCG 诱导的 HepG2 细胞凋亡通过亚 G1 细胞群的积累、磷脂酰丝氨酸的易位、线粒体膜电位的耗竭、DNA 片段化、caspase-3 激活、caspase-9 激活和聚 (ADP-核糖) 得到证实聚合酶裂解。此外,EGCG 增强了对 HepG2 细胞的细胞毒性作用并触发了细胞内活性氧; AKT、JNK、p53信号通路被激活,促进细胞凋亡。 结论:结果表明,EGCG 可能提供有关 EGCG 诱导的 HepG2 细胞凋亡的有用信息,是癌症化疗的合适候选物。

关键词: 表没食子儿茶素-3-没食子酸酯,HepG2,P53,ROS,细胞凋亡,癌症化疗。

图形摘要
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