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首页> 外文期刊>Food and Chemical Toxicology: An International Journal Published for the British Industrial Biological Research >Proanthocyanidins from Uncaria rhynchophylla induced apoptosis in MDA-MB-231 breast cancer cells while enhancing cytotoxic effects of 5-fluorouracil
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Proanthocyanidins from Uncaria rhynchophylla induced apoptosis in MDA-MB-231 breast cancer cells while enhancing cytotoxic effects of 5-fluorouracil

机译:来自undaraia rhynchophylla的原花青素诱导MDA-MB-231乳腺癌细胞中的细胞凋亡,同时增强了5-氟尿嘧啶的细胞毒性作用

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摘要

Breast cancer is the most frequently diagnosed cancer and cause of cancer death in women worldwide. Current treatments often result in systematic toxicity and drug resistance. Combinational use of nontoxic phytochemicals with chemotherapeutic agents to enhance the efficacy and reduce toxicity would be one promising approach. In this study, bioactive proanthocyanidins from Uncaria rhynchophylla (UPAs) were isolated and their anti-breast cancer effects alone and in combination with 5-fluorouracil (5-FU) were investigated in MDA-MB-231 breast cancer cells. The results showed that UPAs significantly inhibited cell viability and migration ability in a dose-dependent manner. Moreover, UPAs induced apoptosis in a dose-dependent manner which was associated with increased cellular reactive oxygen species production, loss of mitochondrial membrane potential, increases of Bax/Bcl-2 ratio and levels of cleaved caspase 3. Treatments of the cells with UPAs resulted in an increase in G2/M cell cycle arrest. Cytotoxic effects of 5-FU against MDA-MB-231 cells were enhanced by UPAs. The combination treatment of UPAs and 5-FU for 48 h elicited a synergistic cytotoxic effect on MDA-MB-231 cells. Altogether, these data suggest that UPAs are potential therapeutic agents for breast cancer. (C) 2017 Elsevier Ltd. All rights reserved.
机译:乳腺癌是全世界癌症最常见的癌症和癌症死亡原因。目前的治疗通常会导致系统的毒性和耐药性。组合使用无毒植物化学症与化学治疗剂,以增强疗效,减少毒性将是一种有希望的方法。在该研究中,在MDA-MB-231乳腺癌细胞中研究了分离出来自植物rhynchophylla(UPAs)的生物活性原花青素(UPAS),并将其抗乳腺癌癌症和5-氟尿嘧啶(5-FU)组合。结果表明,以剂量依赖性方式显着抑制细胞活力和迁移能力。此外,UPAS诱导凋亡以剂量依赖性方式,其与增加的细胞反应性氧物质生产,线粒体膜电位丧失相关,Bax / Bcl-2的比例和切割的caspase的水平增加3.用UPA的细胞处理在G2 / M细胞周期骤停增加。 UPAS增强了5-FU对MDA-MB-231细胞的细胞毒性作用。 UPA和5-FU的组合治疗48 H引发了对MDA-MB-231细胞的协同细胞毒性作用。总的来说,这些数据表明UPA是乳腺癌的潜在治疗剂。 (c)2017 Elsevier Ltd.保留所有权利。

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