文章摘要
张艳霞,丁伟荣,肖祖克.多西紫杉醇对人非小细胞肺癌细胞株A549生长的影响及机制的体外研究[J].江西中医药大学学报,2009,21(1):55-58. |
多西紫杉醇对人非小细胞肺癌细胞株A549生长的影响及机制的体外研究 |
The Inhibitory effect of Docetaxel on the proliferation of human lung cancer cell A549 cells in vitro |
投稿时间:2008-11-04 |
DOI: |
中文关键词: A549细胞株;凋亡;多西紫杉醇;α5β1整合素;Bcl-2;Bax |
英文关键词: |
基金项目: |
张艳霞1,丁伟荣2,肖祖克2 |
1.南昌大学医学院2006级硕士研究生,南昌330031;江西省人民医院呼吸科,南昌330006 |
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中文摘要: |
目的:探讨多西紫杉醇诱导肺癌细胞株A549细胞的生长抑制作用及其对凋亡相关基因表达的影响。方法:采用MTT法测定细胞增殖抑制率,在显微镜下观察细胞凋亡的形态特点,应用流式细胞仪检测细胞凋亡率,采用逆转录聚合酶连反应(RT-PCR)法测定整合素α5β1,bcl-2,bax等凋亡相关基因 mRNA的表达。结果:(1)多西紫杉醇在1.33~108 μg/ml浓度范围内可抑制A549细胞增殖,且此作用与药物浓度、作用时间呈明显相关关系(r=0.947、0. |
英文摘要: |
Objective:To investigate the inhibition effect of Docetaxel on the proliferation of non-small cell lung cancer A549 cell and the corresponding mechanism. Methods: MTT assay was used to determine the proliferation inhibition by Docetaxel to A549 cell. Annexin-V kit was used to test the early apoptosis of A549 cells induced by Docetaxel. The late apoptotic cells were assessed by propidium iodide (PI) staining. Semi-quantitative RT-PCR was employed to measure the expression of VEGF,bFGF ,α5 intergrin submit , β1intergrin submit ,Bcl-2 and Bax。 Results: The proliferation of A549 cells was inhibited significantly by Docetaxel in a concentration-dependent manner and in a time-dependent manner. Docetaxe apoptosis of A549 cells in a concentration -dependent manner(r=0.999,P=0.034).The related level of Bcl-2/Bax andα5 intergrin submit mRNA expression was markedly decreased in A549 cells treated with 12 μg/ml Docetaxel for 24 hours than that in untreated cells(P<0.05),whereas the related expression levels of VEGF,bFGF andβ1 intergrin submit mRNA was not significant between two groups (P﹥0.05). Conclusions: Docetaxel has the inhibition effect to the proliferation of non-small cell lung cancer A549 cell,and induce apoptosis. the suppressed expression of Bcl-2/Bax may be the mechanisms of apoptosis induction,and the suppressed expression of α5β1 intergrin submit may be influence the proliferation, adhesion and metastasis of non-small cell lung cancer. |
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