摘要
耐阿霉素人乳腺癌细胞MCF7adr具多药耐药（Multidxugresistance，MDR）表型。补膏脂抽提剂R3（粉剂）的无细胞毒浓度1：90（2mg／ml）、1：60（3mg／ml）及1：30（6mg／ml），可增加MCF7adr对可霉素（Adriamycin，ADM）的敏感性10．4倍、292倍及730倍。1：90R3＋异搏定（Vera－Pamil，VPL）10μM使MCF7adr对CAM敏感性由10．4倍增至122倍。提示二者有协同作用。流式细胞技术（FCM）显示R3可明显增加MCF7adr细胞内Rh0－123含量。免疫细胞化学技术结果示R3可完全抑制卜糖蛋白（P－glycoprotein，Pgp）表达，是时间依赖性，48小时后MCF7adr细胞Pgp表达完全消失。故提示Ra可能通过抑制Pgp功能，增加ADM在MCF7adr细胞中浓度调控MCF7adr的耐药性。
MCD7adr cell line is a 100-time adriamycin (ADM) resistant human breast cancer cell line with multidrug resistance (MDR) phenotypes. R3 is an powdered extract from a Chinese herb Bu-gu-zhi. Sensitivity to ADM of MCF7adr cells was increased by 10. 4 times, 292 times, 730 times respectively with non-cytotoxicity concentrations of 1: 90 (2mg/ml), 1: 60 (3mg/ml) and 1: 30 (6mg/ml) of the R3. Combining R3 1: 90 with verapamil 10μm, the sensitivity to ADM of MCF7adr cells was increased from 10. 4 times to 122 times. Flowcytometry disclosed that fluorescent intensity of rhodamine-123 (Rho-123) in MCF7adr cells was significantly increased by R3. Immunocytochemistry verified that P-glycoprotein P-gp expressions of MCF7adr cells completely disappeared after 48 hours treated with the R3 1: 60. The results mentioned above showed that the R3 may be a MDR modifier of MCF7adr cells. One of the mechanisms in the authors opinion can be related to depression of the P-gp expression whereby an increase of the ADM accumulation in the cells will occur. There would be a synergistic effect between the R3 and VPL on modulating MDR of MCF7adr cells.
出处
《中国肿瘤临床》
CAS
CSCD
北大核心
1997年第5期325-330,共6页
Chinese Journal of Clinical Oncology
基金
国家"八五"攻关项目
