Flavopiridol在人骨肉瘤多药耐药MNNG/ADM细胞凋亡中的作用及机制  

Effect and mechanism of Flavopiridol on the apoptosis of human osteosarcoma MNNG/ADM cells

作　　者：范姝丽[1] 李旭[1] 林杰[1] 白小涓[1] 

机构地区：[1]中国医科大学附属第一医院,辽宁沈阳110001

出　　处：《山东医药》2009年第3期13-15,共3页Shandong Medical Journal

基　　金：国家自然科学基金科学部主任基金资助项目(30640001)

摘　　要：目的探讨细胞周期蛋白酶抑制剂Flavopiridol对耐阿霉素(ADM)骨肉瘤细胞(MNNG/ADM)增殖抑制及凋亡诱导的作用机制。方法采用MTT法测定ADM及Falvopiridol对骨肉瘤MNNG及MNNG/ADM细胞的半数抑制浓度(IC50),计算其耐药倍数;用流式细胞计数仪(FCM)检测给药后MNNG/ADM周期变化;Western-blotting方法检测细胞中Bcl-2、pro-caspase-3、活化型多聚ADP核糖多聚酶(PARP-85)蛋白水平。结果MNNG及MNNG/ADM细胞增殖明显受抑,凋亡增加,二者的IC50浓度相近;细胞PARP-85(PARP活性型)的表达明显上调,pro-caspase-3及Bcl-2表达下调,其效应具有剂量相关性。结论Flavopiridol可有效诱导MNNG/ADM细胞凋亡,其机制可能与线粒体信号传导途径有关。Objective To investigate the growth-inhibitory and apoptosis inducing effect of Flavopiridol on human Osteosarcoma MNNG/ADM cell and its mechanism in vitro. Methods The IC50 of ADM and Flavopiridol on MNNG and MNNG/ADM cells were determined by using MTT method. Cell cycle progression and apoptosis ratio were determined by using flow cytometry. The expression of Bcl-2, casepase-3 and cleaved-PARP-85 were detected by western blot. Results After exposure to Flavopiridol, the growth of MNNG and MNNG/ADM cells were inhibited. The expression of active-form PARP-85 was up-regulated , and the Bcl-2, and pro-caspase -3 were down-regulated in a dose-dependent manner. Conclusion The apoptosis of MNNG/ADM cells could be induced by Flavopiridol the mechanism maybe related to mitechondrial pathway.

关 键 词：骨肉瘤 多药耐药 细胞凋亡 

分 类 号：R738[医药卫生—肿瘤]