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2'-苯甲酰氧基肉桂醛对耐药癌细胞系的活性。

The activity of 2'-benzoyloxycinnamaldehyde against drug-resistant cancer cell lines.

作者信息

Chung Y M, Yoo Y D, Kim J S, Lee C Y, Kim H J

机构信息

Graduate School of Medicine and Division of Brain Korea 21 Program for Biomedical Science, Seoul.

出版信息

J Chemother. 2007 Aug;19(4):428-37. doi: 10.1179/joc.2007.19.4.428.

Abstract

This study investigated the inhibitory effects of 2'-benzoyloxycinnamaldehyde (BCA) on cancer cells, including various drug-resistant cancer cell lines. To observe this activity, the anticancer drug-resistant cell lines were established by continuously exposing the parental cells to 5-fluorouracil (5-FU) and cyclophosphamide (CDDP), and examining the cells with the MTT assay and flow cytometric analysis. The BCA treatment produced similar growth inhibitory effects and apoptotic cell death on the drug-resistant cancer cells as their parental cells. The activation of the p38-mitogen activated protein kinase, an increased level of reactive oxygen species (ROS) generation and downregulation of Bcl-2 were observed in both the drug resistant and non-drug resistant cell lines. The GSH treatment effectively inhibited BCA-induced apoptosis by blocking ROS generation, suggesting that ROS is a major regulator in BCA-induced apoptotic cell death. These results suggest that BCA can be a useful drug candidate for treating drug-resistant cells.

摘要

本研究调查了2'-苯甲酰氧基肉桂醛(BCA)对癌细胞的抑制作用,包括各种耐药癌细胞系。为观察这种活性,通过将亲代细胞持续暴露于5-氟尿嘧啶(5-FU)和环磷酰胺(CDDP),并采用MTT法和流式细胞术分析对细胞进行检测,从而建立抗癌耐药细胞系。BCA处理对耐药癌细胞产生了与亲代细胞相似的生长抑制作用和凋亡性细胞死亡。在耐药和非耐药细胞系中均观察到p-38丝裂原活化蛋白激酶的激活、活性氧(ROS)生成水平的增加以及Bcl-2的下调。谷胱甘肽(GSH)处理通过阻断ROS生成有效抑制了BCA诱导的凋亡,这表明ROS是BCA诱导凋亡性细胞死亡的主要调节因子。这些结果表明,BCA可能是一种治疗耐药细胞的有用候选药物。

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