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210.4 μg/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324.9 μg/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 proteasorae inhibitor bortezomib could sensitize leukemia drug - resistant 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: IC50of pharmorubicin alone and in combination with bortezomib on K562/DNR was 417.0μg/ml and 210. 4μg/ml respectively, 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 couldrnincrease 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 reverse durg resistance.
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