Chlorogenic acid induces reactive oxygen species generation and inhibits the viability of human colon cancer cells

Chlorogenic acid induces reactive oxygen species generation and inhibits the viability of human colon cancer cells
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DOI:
10.1097/cad.0000000000000430
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发表时间:
2017-01-01
期刊:
影响因子:
2.3
通讯作者:
Li, Jie
Li, Jie
中科院分区:
医学4区
文献类型:
--
作者:
Hou, Ni;Liu, Na;Li, Jie

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绿原酸(Chlorogenic Acid,CGA)是一种在人类饮食中发现的多酚类物质。以前的研究表明,CGA对肝脏疾病起着保护作用。结肠在CGA代谢中起着关键作用。然而,关于CGA在结肠癌中的直接作用和潜在的分子机制知之甚少。在这里,我们研究这些机制的CGA活动在人类结肠癌细胞。采用MTT法检测CGA对人结肠癌细胞株HCT 116和HT 29细胞活力的影响。采用荧光显微镜和流式细胞仪检测细胞内活性氧(ROS)的含量。此外,通过细胞周期分析检测细胞增殖的变化。免疫印迹分析用于观察潜在的分子变化。CGA以剂量依赖性方式抑制HCT 116和HT 29细胞的活力。CGA诱导ROS产生,而ROS清除剂N-乙酰半胱氨酸的组合使用衰减的CGA诱导的活力抑制。此外,CGA诱导细胞周期停滞在S期,并抑制细胞外信号相关激酶的激活,在这两种细胞类型中,这可能有助于ROS诱导的CGA处理引起的活力抑制。CGA诱导的ROS产生抑制人结肠癌细胞的细胞活力。CGA引起S期阻滞和细胞外信号相关激酶失活,这可能导致观察到的活力抑制。因此,CGA是一种潜在的治疗CRC的方法。版权所有(C)2016威科医疗集团All rights reserved.
Chlorogenic acid (CGA) is one of the polyphenols identified in the human diet. Previous studies have shown that CGA plays a protective role against liver diseases. The colon plays a pivotal role in CGA metabolism. However, little is known about the direct effects and the underlying molecular mechanisms of CGA in colon cancer. Here, we investigate these mechanisms of CGA activity in human colon cancer cells. The effects of CGA on the viability of two human colon cancer cell lines, HCT116 and HT29, were determined using the MTT assay. The intracellular reactive oxygen species (ROS) were detected using fluorescence microscopy and flow cytometry. In addition, changes in cell proliferation were detected by cell cycle analysis. Immunoblotting analysis was used to observe the underlying molecular changes. CGA inhibited the viability of HCT116 and HT29 cells in a dose-dependent manner. CGA induced ROS production, whereas the combined use of ROS scavenger N-acetylcysteine attenuated the CGA-induced viability inhibition. Moreover, CGA induced cell cycle arrest at the S phase and suppressed the activation of extracellular signalrelated kinase in both cell types, which likely contributes toward the ROS-induced viability inhibition caused by CGA treatment. CGA-induced ROS production inhibited cell viability in human colon cancer cells. CGA caused S-phase arrest and extracellular signal-related kinase inactivation that may have led to the observed viability inhibition. CGA is therefore a potential treatment against CRC. Copyright (C) 2016 Wolters Kluwer Health, Inc. All rights reserved.