摘要
目的:观察蛋白酶体抑制剂硼替佐米是否可以增加耐药白血病细胞株K562/DNR对化疗药物的敏感性。方法:MTT法计算硼替佐米逆转耐药倍数,流式细胞术(FCM)检测细胞调亡比及细胞内药物浓度。结果:表柔比星单独及联合硼替佐米作用于K562/DNR细胞株的IC50分别为417.0μg/ml和210.4μg/ml,逆转倍数为1.98倍;柔红霉素单独及联合硼替佐米作用于K 562/DNR细胞株的IC50分别为457.7μg/ml和324.9μg/ml,逆转倍数为1.4倍。单独应用表柔比星组细胞调亡比为(28.74±4.6)%,联合硼替佐米组细胞调亡比为(39.14±9.6)%。硼替佐米能使K562/DNR细胞内柔红霉素含量增加,而对K562/S细胞无类似影响。结论:蛋白酶体抑制剂硼替佐米能增加耐药白血病细胞株K562/DNR的化疗药物的敏感性,逆转耐药性。
Objective:To observe whether proteasome inhibitor bortezomib could sensitize leukemia drug - resist- ant cell line K562/DNR to chemical durgs. Methods:Resistance reverse fold of bortezomib was calculated according to MTT assay,and apoptosis rates of cells and durg concentration were observed by flow cytometry. Results: IC50 of pharmorubicin alone and in combination with bortezomib on K562/DNR was 417.01μg/ml and 210.4μg/ml respec- tively,and reverse fold was 1.98;IC50 of daunorubicin alone and in combination of bortezomib on K562/DNR was 457.7μg/ml,and 324.9μg/ml respectively and reverse fold was 1.4. Apoptosis under treatment of pharmorubicin a- lone and in combination of bortezomib was (28.74± 4.6) % and (39.14 ± 9.6) % respectively. Bortezomib couldincrease intracellular daunorubicin amount of K562/DNR and had no similar influence on K562/S. Conclusion:Pro- teasome inhibitor bortezomib could sensitize leukemia drug - resistant cell line K562/DNR to chemical durgs and re- verse durg resistance.
出处
《现代肿瘤医学》
CAS
2013年第3期474-477,共4页
Journal of Modern Oncology
基金
辽宁省教育厅课题(编号:20060985)
关键词
硼替佐米
耐药
凋亡
白血病
botezomib
resistance
apoptosis
leukemia