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目的 观察 bcl- x L 基因可否介导白血病细胞的多药耐药 ,并探讨其机制 .方法 采用脂质体法将 bcl- x L c DNA转导入 HL- 6 0细胞 ;免疫印迹法检测 Bcl- x L 及抗凋亡蛋白Bax的表达 ;MTT法测定足叶乙甙、柔红霉素、阿霉素对转染细胞的细胞毒性 ;流式细胞仪定量检测凋亡细胞及细胞内药物浓度 .结果 Bcl- x L高表达可抑制足叶乙甙诱发的凋亡 ,抑制率为 40 .5 % ;降低上述化疗药物的细胞毒作用 ,耐药指数分别为 3.2 ,3.2 ,1 .6 ;但细胞内柔红霉素药物浓度无改变 .结论 Bcl- x L可能作为一种新的耐药途径 ,通过抑制化疗药物诱发的细胞凋亡参与多药耐药的形成 .
Objective To investigate whether bcl-x L gene can mediate multidrug resistance in leukemia cells and to explore its mechanism. Methods Liposome method was used to transfer bcl-x L c DNA into HL-60 cells; Western blotting was used to detect Bcl- Expression of x L and anti-apoptosis protein Bax; MTT assay was used to determine the cytotoxicity of etoposide, daunorubicin, and doxorubicin in transfected cells; flow cytometry was used to quantitatively detect apoptotic cells and intracellular drug concentration. Results The high expression of Bcl-xL could inhibit the apoptosis of E. aethioae, the inhibition rate was 40.5%, and the cytotoxicity of the above-mentioned chemotherapeutic drugs was reduced. The drug resistance index was 3.2, 3.2, 1.6, respectively. There was no change in the concentration of daunorubicin. Conclusion Bcl-xL may act as a new drug resistance pathway and participate in the formation of multidrug resistance by inhibiting apoptosis induced by chemotherapeutic drugs.