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黄芪多糖对人肺癌A549 细胞增殖的作用及其机制的实验研究
引用本文:刘爱平,曾峰. 黄芪多糖对人肺癌A549 细胞增殖的作用及其机制的实验研究[J]. 肿瘤药学, 2011, 0(6): 499-501,507
作者姓名:刘爱平  曾峰
作者单位:[1]湖南省郴州市疾病预防控制中心,湖南郴州423000 [2]湖南师范大学生命科学院,湖南长沙410081
摘    要:目的探讨黄芪多糖(astragalus polysaccharide,APS)对人肺癌A549细胞增殖的作用及其机制。方法用不同浓度的APS(25μg.mL-1、50μg.mL-1、10μg.mL-1、200μg.mL-1、400μg.mL-1)作用于人肺癌A549细胞,用MTT法检测细胞增殖的抑制率,免疫细胞化学法检测bcl-2和bax的表达。结果 APS的浓度在25μg.mL-1~400μg.mL-1范围内均可抑制人肺癌A549细胞的增殖,100μg.mL-1的APS对A549细胞增殖的抑制率达最高,100μg.mL-1的APS作用于人肺癌A549细胞48和72小时后,均可下调bcl-2和上调bax的表达。结论 APS能够可抑制人肺癌A549细胞的增殖,可能与其下调bcl-2和上调bax的表达有关。

关 键 词:黄芪多糖  人肺癌A549细胞  细胞增殖  bcl-2  bax

Experimental study on the effect and mechanisms of astragalus polysaccharide on the proliferation of human lung cancer cell line A549
--. Experimental study on the effect and mechanisms of astragalus polysaccharide on the proliferation of human lung cancer cell line A549[J]. Anti-Tumor Pharmacy, 2011, 0(6): 499-501,507
Authors:--
Affiliation:1 Center for Disease Control and Prevention of Chenzhou,Hunan province,Chenzhou,423000;2College of life sciences of Hunan Normal University,Changsha,Hunan,410081)
Abstract:Objective To investigate the effect and mechanisms of APS on proliferation of human lung cancer cell line A549.Method Cells were treated with different concentrations of APS(25μg.mL-1,50 μg.mL-1,100 μg.mL-1,200μg.mL-1,400μg.mL-1).The inhibitory rate of A549 cell proliferation was detected by MTT and the expression of Bcl-2 and bax were tested by immunocytochemistry.Results APS inhibited the proliferation of A549 cells within 25μg.mL-1~400μg.mL-1.APS at a concentration of 100 μg.mL-1 significantly inhibited the proliferation of A549 cells.The expression of bcl-2 was down-regulated and the expression of bax was up-regulated in A549 cells after treated by the APS at a concentration of 100μg.mL-1for 48 and 72 hours.Conclusion APS was able to inhibit the proliferation of A549 cells,the downregulation of bcl-2 and upregulation of bax may be involved in this effect.
Keywords:Astragalus polysaccharide  Human lung cancer A549 cell line  Cell proliferation  Bcl-2  Bax
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