摘要
目的 研究肿瘤坏死因子 (TNFα)和足叶乙甙 (VP16 )联合对肺癌细胞包株的作用及其机制。方法 用MTT法检测不同浓度的TNFα、VP16及TNFα联合VP16对人肺癌细胞系A5 4 9的细胞毒作用以及用间接荧光标记法、流式细胞仪观察TNFα、VP16及TNFα联合VP16对A5 4 9的细胞周期、粘附分子表达的影响。结果 TNFα、VP16对A5 4 9细胞的生长抑制作用有剂量依赖关系 ,而TNFα联合VP16对A5 4 9抑制作用较TNFα、VP16作用显著 (P <0 .0 1)。TNFα、TNFα联合VP16能上调CD5 4表达 ,与VP16均能上调CD95表达 ,而粘附分子CD11α、CD18、CD4 0、CD80、CD137等用药后仍不表达。对细胞周期用药后G2 期明显下降 (13.2 %下降至 3.0 % ) ,S期上升 (2 7.3%上升至 4 2 .5 % )。结论 TNFα联合VP16增加A5 4 9的抑制率 ,增强CD5 4、CD95表达。推测TNFα联合VP16对A5 4 9细胞的作用是通过抑制DNA合成及有丝分裂 ,使G0 +G1+S期不能及时转至G2 。
Objective To investigate the cytotoxic activities of tumor necrosis factor-α and VP16 on human lung cancer line cells A549 and the expression of adhesive molecules on the surface of the cells.Methods A wide range of TNFα concentration (from 10～160ng/ml) and VP16 (10-80μmol/L) were tested using the MTT assay.The expressions of adhesive molecules on the surface of A549 cells were measured by flow cytometric analysis (FCM).Results Data showed that the suppressive effects of TNFα and VP16 on A549 were dose-dependent and the suppressive effect of TNFα combined with VP16 was better than that of TNFα or VP16.respectively,TNFα with VP16 significantly up-regulated the expressions of CD54?CD95.But there were no changes among CD40?CD80?CD11α?CD18?CD137.After 4 hours exposure of A549 cell to TNFα and VP16,the cycle of cells shifted from G 2 phase to S phase.Conclusion TNFα with VP16 could inhibit the proliferation of A549 cells and enhance the expressions of some adhesive molecules on the surface of A549 cells.It is suggested that the mechanism of TNFα with VP16 on tumor cell is to interfere with the cycle and induce apoptosis of A549.
出处
《苏州大学学报（医学版）》
CAS
2002年第4期368-372,共5页
Suzhou University Journal of Medical Science
