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目的 :探讨白血病细胞多药耐药 (MDR)与细胞凋亡的关系。方法 :在体外用化疗药物阿霉素 (ADM)诱导白血病细胞株 K5 6 2 MDR的产生 ,用 As2 O3诱导细胞的凋亡 ,采用流式细胞仪检测细胞表面 P糖蛋白 (P- gp)的表达 ;荧光定量 PCR检测 MDR1 m RNA;通过流式细胞仪检测Anexin- V判断凋亡细胞数量的多少 ;观察 MDR与细胞凋亡的关系。结果 :5 μm ol/ L 的 ADM能诱导 K5 6 2细胞 MDR的产生 ,随着作用时间的延长 ,P- gp/ MDR1 m RNA的表达逐渐升高 ;P- gp/MDR1 m RNA的表达与细胞凋亡呈负相关 (r=0 .6 8,P<0 .0 1 ) ;在 As2 O3作用下 ,细胞凋亡增加的同时 ,P- gp的表达下调。结论 :抗癌药物能诱导白血病细胞 MDR的产生 ,细胞的耐药性与凋亡抑制相关 ,诱导细胞的凋亡能减低白血病细胞的 MDR。
Objective: To investigate the relationship between multidrug resistance (MDR) and apoptosis in leukemia cells. Methods: The chemotherapeutic drug adriamycin (ADM) was used to induce the proliferation of K562 MDR cells in vitro. The cell apoptosis was induced by As2 O3. The expression of P-glycoprotein (P-gp) was detected by flow cytometry The expression of MDR1 m RNA was detected by real-time PCR. Anexin-V was used to determine the number of apoptotic cells by flow cytometry. The relationship between MDR and apoptosis was observed. Results: 5 μmol / L ADM induced the MDR production in K562 cells. The expression of P-gp / MDR1 m RNA gradually increased with the prolongation of time. The expression of P- Apoptosis was negatively correlated (r = 0.68, P <0.01). Under the action of As2 O3, apoptosis increased while P-gp expression was down-regulated. Conclusion: The anticancer drugs can induce MDR in leukemia cells. The drug resistance of the cells is related to the inhibition of apoptosis. Inducing the apoptosis of cells can reduce the MDR of leukemia cells.