白藜芦醇对肺癌紫杉醇耐药细胞的增殖抑制作用及其机制

doi:10.3969/j.issn.1004-616x.2018.03.007

癌变·畸变·突变 ›› 2018, Vol. 30 ›› Issue (3): 200-203,208.doi: 10.3969/j.issn.1004-616x.2018.03.007

白藜芦醇对肺癌紫杉醇耐药细胞的增殖抑制作用及其机制

吴异兰¹, 王晗²

1. 福建中医药大学护理学院, 福建福州 350122;
2. 福建医科大学附属协和医院肿瘤科, 福建福州 350001

收稿日期:2017-11-27 修回日期:2018-03-12 出版日期:2018-05-30 发布日期:2018-05-30
作者简介:吴异兰,E-mail:yilanwu@163.com
基金资助:
福建省自然科学基金项目（2017J01831）

Inhibition of proliferation by resveratrol in paclitaxel-resistant lung adenocarcinoma cells

WU Yilan¹, WANG Han²

1. School of Nursing, Fujian University of Traditional Chinese Medicine, Fuzhou 350122;
2. Department of Medical Oncology, Fujian Medical University Union Hospital, Fuzhou 350001, Fujian, China

Received:2017-11-27 Revised:2018-03-12 Online:2018-05-30 Published:2018-05-30

摘要/Abstract

摘要： 目的：研究白藜芦醇作用后人肺腺癌紫杉醇耐药细胞对紫杉醇敏感性的改变，并探讨其作用机制。方法：建立人肺腺癌紫杉醇耐药细胞A549/Taxol-R，用不同浓度白藜芦醇、紫杉醇单独或联合干预A549/Taxol-R细胞，MTT法检测细胞增殖抑制率；概率单位法计算半数抑制浓度（IC₅₀）；观察不同浓度白藜芦醇处理后，紫杉醇对A549/Taxol-R细胞IC₅₀的变化；流式细胞术检测细胞凋亡水平；Western blot检测凋亡相关蛋白Bax、Bcl-2和Caspase-3的表达。结果：白藜芦醇对A549/Taxol-R细胞增殖的抑制率具有浓度和时间的双重依赖性（P均 < 0.05）。白藜芦醇处理后，紫杉醇对A549/Taxol-R细胞的IC₅₀值下降，从（17.50±1.24）μg/mL降低至（4.18±0.62）μg/mL。白藜芦醇和紫杉醇联合干预的A549/Taxol-R细胞凋亡率、坏死率高于单独干预组（P < 0.05），联合干预组A549/Taxol-R细胞的Bax、Caspase-3的表达较单独干预组上调，而Bcl-2的表达则相对下调（P < 0.05）。结论：白藜芦醇可能通过促进细胞的凋亡来增强人肺腺癌紫杉醇耐药细胞对紫杉醇的敏感性，其机制可能和促进Bax、Caspase-3的表达，下调Bcl-2的表达有关。

关键词: 肺癌, 化疗耐药, 紫杉醇, 白藜芦醇

Abstract: OBJECTIVE: To study mechanisms in sensitivity of paclitaxel-resistant human lung adenocarcinoma cells from treatment with resveratrol. METHODS: A549/Taxol-R,a human lung adenocarcinoma cell line that resist paclitaxel,was established and treated with different concentrations of resveratrol and paclitaxel alone or in combination. MTT assay was performed and SPSS was used to calculate IC₅₀ of A549/Taxol-R to paclitaxel. Change of IC₅₀ was determined after treatment with resveratrol at different concentrations. Apoptosis rates were detected with flow cytometry. Expressions of Bax,Bcl-2 and Caspase-3 were detected by Western blot. RESULTS: The inhibitory rate of resveratrol to A549/Taxol-R cells was dependent on concentration and time. After treated with resveratrol,the IC₅₀ of paclitaxel on A549/Taxol-R cells decreased from (17.50±1.24) μg/mL to (4.18±0.62) μg/mL. The apoptosis and necrosis rates of A549/Taxol-R cells that were treated with combined resveratrol and paclitaxel were higher than those that treated with single drugs (P < 0.05). Expression of Bax and Caspase3 in the combined treatment group was higher than that in the single treatment group,while expression of Bcl-2 was relatively down-regulated (P < 0.05). CONCLUSION: Resveratrol may increase sensitivity of paclitaxel-resistant human lung adenocarcinoma cells to paclitaxel by promoting cell apoptosis. The mechanism may be related to promotion of expression of Bax and Caspase3 and down-regulation of Bcl-2 expression.

Key words: lung cancer, drug resistance, paclitaxel, resveratrol

中图分类号:

R734.2

吴异兰, 王晗. 白藜芦醇对肺癌紫杉醇耐药细胞的增殖抑制作用及其机制[J]. 癌变·畸变·突变, 2018, 30(3): 200-203,208.

WU Yilan, WANG Han. Inhibition of proliferation by resveratrol in paclitaxel-resistant lung adenocarcinoma cells[J]. Carcinogenesis, Teratogenesis & Mutagenesis, 2018, 30(3): 200-203,208.

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白藜芦醇对肺癌紫杉醇耐药细胞的增殖抑制作用及其机制

Inhibition of proliferation by resveratrol in paclitaxel-resistant lung adenocarcinoma cells

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