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机构地区:[1]上海交通大学医学院附属仁济医院核医学科,上海200127
出 处:《肿瘤》2013年第4期299-303,共5页Tumor
基 金:国家自然科学基金资助项目(编号:81071180);国家重点基础研究发展计划(编号:2012CB932600);国家科技重大专项课题(编号:2012ZX09506001-005)
摘 要:目的:探讨人肺腺癌细胞株A549及其紫杉醇耐药细胞株A549/taxol之间葡萄糖代谢的差异,以及二氯乙酸盐(dichloroacetate,DCA)对这2种细胞葡萄糖代谢的影响。方法:首先采用CCK-8法检测A549及A549/taxol细胞对紫杉醇的耐药性。再用液体闪烁仪检测A549和A549/taxol细胞摄取14C-葡萄糖后CO2的产生和脂质的生成情况。另外,分别用γ计数器和乳酸测定试剂盒检测18氟-2-脱氧-β-D-葡萄糖(18F-2-deoxy-β-D-glucose,18F-FDG)摄取和乳酸产生情况。结果:A549/taxol细胞摄取6-14C-葡萄糖后CO2释放量、18F-FDG摄取率和乳酸生成量均低于A549细胞。A549细胞经DCA处理后6-14C-葡萄糖释放的CO2水平升高,而A549/taxol细胞经DCA处理后6-14C-葡萄糖释放的CO2量无变化。结论:A549/taxol细胞有一定的线粒体氧化呼吸抑制作用。DCA能促进A549细胞线粒体的氧化呼吸作用,而对其耐药株A549/taxol细胞的氧化呼吸作用不大。Objective: To investigate the difference in glucose metabolism between lung adenocarcinoma A549 cell line and its taxol-resistant (A549/taxol) cell line, and to determine the effect of DCA (dichloroacetate) on glucose metabolism of these two cell lines. Methods: The taxol resistance of A549 and A549/taxol cell lines were firstly determined by CCK-8 (cell counting kit-8) assay. Then the productions of CO2 and lipid in A549 and A549/taxol cells were detected by scintillation counter after treatment with ^14C-qlucose. Furthermore, the uptake of ^18F-FDG (^18F-2-deoxy-β-D-glucose) and the production of lactate were detected by y-counter and lactate measurement kit, respectively. Results: All of CO2 production level, the ^18F-FDG uptake rate and the lactate production level after treatment with 6-^14C-glucose were lower in A549/taxol cells than those in A549 cells. The level of C02 production after treatment with 6-^14C-glucose was significantly higher in A549 cells treated with DCA than that in A549 cells without DCA treatment. However, DCA had no effect on the CO2 production after treatment with 6-^14C-glucose in A549/taxol cells. Conclusion: There is a certain extent of mitochondrial oxidative breathing suppression in A549/taxol cells. DCA can promote mitochondrial oxidative respiration in A549 cells, but has no effect on that in A549/taxol cells.
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