绿茶儿茶素增强阿霉素对BE(2)C神经母细胞瘤细胞的体外作用

IF 1 Q4 PHARMACOLOGY & PHARMACY
Z. Bakhtiari, L. Delphi, H. Sepehri, N. Motamed
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引用次数: 0

摘要

背景:神经母细胞瘤(NB)是一种恶性交感神经系统肿瘤,是第二常见的儿童肿瘤类型。增加NB死亡人数是设计NB治疗新策略的必要条件。目前,天然化合物因其诱导细胞凋亡的能力而逐渐得到开发。茶儿茶素是一种黄酮类化合物,是抑制肿瘤生长和促进肿瘤细胞凋亡的天然组合之一。在本研究中,研究了纯儿茶素、阿霉素(DOX)及其组合对NB [BE(2)C细胞]细胞模型的影响。恶性交感神经系统癌是儿童肿瘤的第二常见类型。增加NB死亡人数是设计NB治疗新策略的必要条件。目前,天然化合物因其诱导细胞凋亡的能力而逐渐得到开发。茶儿茶素是一种黄酮类化合物,是抑制肿瘤生长和促进肿瘤细胞凋亡的天然组合之一。目的:在本研究中,研究了纯儿茶素、阿霉素(DOX)及其联合使用对NB [BE(2)C细胞]细胞模型的影响。方法:采用3-(4,5-二甲基噻唑-2-基)-2,5-二苯基- 2h -溴化四唑(MTT)法测定各药物的反应剂量。荧光显微镜和细胞周期分析检测细胞凋亡。最后,进行菌落形成以检测细胞的迁移和侵袭。结果:MTT实验显示儿茶素和DOX处理均抑制细胞活力,无效剂量联合使用具有更强的细胞毒作用。然而,这些处理不能抑制正常人成纤维细胞的生长。此外,这种结合减少了细胞附着、染色质断裂和细胞周期中的G/S阻滞。克隆实验表明,10天后菌落大小和数量明显减少;因此,Catchin及其与DOX的结合抑制了细胞克隆形成和迁移的能力。结论:儿茶素、DOX及其联合使用可抑制体外BE(2)C神经母细胞瘤细胞的增殖、侵袭和迁移,并通过阻滞细胞周期诱导细胞凋亡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Green Tea Catechin Potentiating Doxorubicine Effects against BE(2)C Neuroblastoma Cells In Vitro
Background: Neuroblastoma (NB), a malignant sympathetic nervous system cancer, is the second most common type of pediatric tumor. Increasing the number of NB death emerges to design a new strategy for NB treatment. Nowadays, the development of natural compounds has gradually increased due to their ability to apoptosis induction. Tea catechin, a flavonoid compound, is one of the natural combinations which inhibit tumor growth and enhance tumor cell apoptosis. In the current study, the effects of pure catechin, doxorubicin (DOX), and their combination on a cellular model of NB [BE(2)C cells] are perused. (NB) a malignant sympathetic nervous system cancer is the second most common type of pediatric tumor. Increasing the number of NB death emerges to design a new strategy for NB treatment. Nowadays, the development of natural compounds has gradually increased due to their ability to apoptosis induction. Tea catechin, a flavonoid compound, is one of the natural combinations which inhibit tumor growth and enhance tumor cell apoptosis. Objectives: In the current study, the effects of pure catechin, doxorubicin (DOX), and their combination on a cellular model of NB [BE(2)C cells] are perused. Methods: The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay was done to assess a response dose for each drug. Fluorescent Microscopic and cell cycle analyses were performed for apoptosis detection. Finally, Colony formation was performed to examine cell migration and invasion. Results: The MTT assay showed that catechin and DOX treatment inhibited the viability of the cells while the combination of their ineffective doses had more cytotoxic effects. However, these treatments could not inhibit the cell growth of the normal human fibroblast. Moreover, this combination reduced cell attachment, chromatin fragmentation, and G/S arrest in the cell cycle. The clonogenic assay demonstrated that colony size and numbers obviously reduced after ten days; therefore, Catchin and its combination with DOX suppressed cell capacities of clone formation and migration. Conclusions: These results suggest that catechin, DOX, and their combination may inhibit the proliferation, invasion, and migration of BE(2)C neuroblastoma cells in vitro while inducing cell apoptosis by arresting the cell cycle.
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CiteScore
1.40
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