中文摘要：

目的探讨正常骨髓基质细胞对残留耐药Jurkat细胞凋亡的促进作用及其可能机制。方法体外分离培养急性淋巴细胞白血病患者和健康供者骨髓基质细胞（BMSCs）,分别模拟白血病和正常骨髓造血微环境,并与获得柔红霉素（DNR）耐药的Jurkat细胞（Jurkat/DNR细胞）共培养。绘制悬浮培养和与BMSCs共培养4d的Jurkat/DNR细胞的增殖曲线,并检测悬浮培养及共培养14、1、0d的Jurkat/DNR细胞的caspase3/7活性和bcl-2、bax、DAPK1 mRNA表达情况。结果与骨髓基质细胞共培养比较,悬浮培养的Jurkat/DNR细胞生长受到明显抑制。共培养41、0d后,Jurkat/DNR细胞caspase3/7活性升高,且共培养10d的活性高于共培养4d（P〈0.05）。共培养4、10d后,Jurkat/DNR细胞bcl-2表达增加,共培养14、1、0d后,死亡相关蛋白激酶1（DAPK1）表达增加（P〈0.05）。而bax表达在各时间点间差异无统计学意义（P〉0.05）。结论正常骨髓基质细胞能促进Jurkat/DNR凋亡,其机制可能与过表达的DAPK1诱导Jurkat/DNR细胞凋亡和bcl-2转录下调c、aspase3/7活性升高有关。

英文摘要：

Objective To investigate the effect in vitro of normal bone marrow stromal cells on promoting apoptosis of residual daunorubicin-resistant Jurkat cells and the possible mechanism.Methods The bone marrow stromal cells（BMSCs） were isolated from the patients with acute leukemia and the healthy volunteers,and then cultivated in vitro to simulate the hematopoietic microenvironment of leukemia and normal bone marrow,and co-cultivated with Jurkat/DNR cells,the Jurkat cells with DNR resistance.The proliferation curves of Jurkat/DNR cells cultured with and without normal BMSCs for 4 days were drawn.The caspase3/7 activity and the expressions of bcl-2,bax,death-associated protein kinase1（DAPK1） mRNA of the Jurkat/DNR cells after suspension culture,co-cultured with normal BMSCs for 1d,4d and 10d were detected.Results Compared with the Jurkat/DNR cells co-cultured with normal BMSCs,the proliferation of suspension cultured Jurkat/DNR cells were remarkably inhibited.The caspase3/7 activity of Jurkat/DNR cells increased after co-cultured for 4 and 10 days,and the activity was higher at co-cultured for 10 days than for 4 days（P〈0.05）.The expression of bcl-2 mRNA increased after co-cultured for 4 and 10 days,and the expression of DAPK1 mRNA increased after co-cultured for 1,4 and 10 days（P〈0.05）.There was no significant difference in the bax mRNA expression between the Jurkat/DNR cells with different culturing methods（P〉0.05）.Conclusion The normal BMSCs may promote the apoptosis of Jurkat/DNR cells.The mechanism may be related to the over expression of DAPK1,which may induce the apoptosis of Jurkat/DNR cells,down regulate the transcription of bcl-2 and increase the activity of caspase3/7.