中文摘要：

目的：探讨蛋白酶体抑制剂（PSI）对t（8；21）急性髓系白血病治疗的分子生物学机制。方法：t（8；21）白血病细胞Kasumi-1经5，8，10，25，50nmol／LPSI处理后，进行细胞计数和MTT检测，并且使用流式细胞分选和蛋白免疫印迹方法检测不同浓度的药物处理下细胞的调亡情况。结果：蛋白酶体抑制剂PSI诱导t（8；21）白血病细胞Kasumi-1在5～50nmol／L时间浓度梯度的自血病细胞调亡，以及对患者细胞有抑制增长作用，并发现随着药物作用时间的延长，表征凋亡的caspase．3条带的切割随之愈加的显著。这些结果表明，PSI诱导的细胞凋亡是通过caspase-3激活凋亡途径。结论：PSI可能是一个潜在的治疗t（8；21）白血病，并通过靶向AML1-ETO蛋白和激活凋亡通路治疗白血病的有效药物。

英文摘要：

Objective To investigate the molecular biological mechanism of proteasome inhibitor （PSI） in treating t（ 8;21 ） （q22 ;q22） acute myeloid leukemia（AML）. Methods Kasumi-1 cells were treated with different concentrations （5,8,10, 25,50 nmol/L） of PSI for different times ,and the cell numbers were counted and the cell vitality were detected by MTT. The apoptosis of cells were detected by flow cytometry and Western blot. Results In the range from 5 to 50 nmol/L,PSI induced the cell apoptosis and inhbited the growth of Kasumi-1 cells in patients with AML, meanwhile the degradation band of caspase-3 protein representing cell apoptosis was more obviously induced following the prolongation of treatment time, suggesting that PSI induced apoptosis of AML cells through activating caspase-3 apoptotie pathways. Conclusion PSI may be a potential drug for treatment of t （ 8 ; 21 ） leukemia through targeting AML1 -ETO protein and activating caspase-3 apoptotie pathway.