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Cytotoxicity, Oxidative Stress, Cell Cycle Arrest, and Mitochondrial Apoptosis after Combined Treatment of Hepatocarcinoma Cells with Maleic Anhydride Derivatives and Quercetin

机译:用马来酸酐衍生物和槲皮素组合治疗肝癌细胞组合治疗后细胞毒性,氧化应激,细胞周期滞留和线粒体凋亡

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摘要

The inflammatory condition of malignant tumors continually exposes cancer cells to reactive oxygen species, an oxidizing condition that leads to the activation of the antioxidant defense system. A similar activation occurs with glutathione production. This oxidant condition enables tumor cells to maintain the energy required for growth, proliferation, and evasion of cell death. The objective of the present study was to determine the effect on hepatocellular carcinoma cells of a combination treatment with maleic anhydride derivatives (prooxidants) and quercetin (an antioxidant). The results show that the combination of a prooxidant/antioxidant had a cytotoxic effect on HuH7 and HepG2 liver cancer cells, but not on either of two normal human epithelial cell lines or on primary hepatocytes. The combination treatment triggered apoptosis in hepatocellular carcinoma cells by activating the intrinsic pathway and causing S phase arrest during cell cycle progression. There is also clear evidence of a modification in cytoskeletal actin and nucleus morphology at 24 and 48 h posttreatment. Thus, the current data suggest that the combination of two anticarcinogenic drugs, a prooxidant followed by an antioxidant, can be further explored for antitumor potential as a new treatment strategy.
机译:恶性肿瘤的炎症状况不断地将癌细胞暴露于反应性氧物质,导致抗氧化防御系统的活化的氧化条件。谷胱甘肽生产发生类似的活化。此氧化剂条件能够使肿瘤细胞对维持生长,增殖和细胞死亡的逃避所需的能量。本研究的目的是确定用马来酸酐衍生物(促乙酸)和槲皮素(抗氧化剂)的组合处理的肝细胞癌细胞的影响。结果表明,过氧化物/抗氧化剂的组合对HUH7和HEPG2肝癌细胞具有细胞毒性作用,但不在两种正常人体上皮细胞系或原发性肝细胞中的任何一种。通过激活内在途径并在细胞周期进展期间引起S期阻滞来触发肝细胞癌细胞中的细胞凋亡。还有明确的证据表明在24和48小时的24和48小时的细胞骨架肌动蛋白和核形态的修饰。因此,目前的数据表明,可以进一步探索两种抗毒性药物,抗氧化剂后跟抗氧化剂的组合,作为一种新的治疗策略。

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