摘要
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 .
AIM To observe whether the overexpression of Bcl xL in HL 60 cells, which were transfected with bcl xL cDNA, can confer the multidrug resistance and explore its mechanism. METHODS bcl xL cDNA was transfected into HL 60 cells using lipofectamine and the expressions of Bcl xL and Bax in transfected cells were defined with Western analysis. Drugs sensitivity was compared by MTT cytotoxicity assay and apoptotic cell rate was quantitatively analyzed with FCM. The concentration of daunorubicin was measured with FCM. RESULTS The transient overexpression of Bcl xL inhibited the etoposide induced apoptosis by 40.5% and decreased the sensitivity of HL 60 cells to etoposide, daunorubicin and adriamycin. The resistance factors were 3.2 , 3.2 and 1.6 respectively. The concentrations of daunorubicin were the same in transfected and control cells. CONCLUSION bcl xL gene might be a new multidrug phenotype. It can confer the drug resistance in the transfected bcl xL cells by inhibiting the apoptosis.
出处
《第四军医大学学报》
2000年第1期45-47,共3页
Journal of the Fourth Military Medical University
基金
国家自然科学基金!( 3 940 0 0 5 7)
