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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。
AIM: To investigate the differences in glucose metabolism between human lung adenocarcinoma cell line A549 and its paclitaxel-resistant cell line A549 / taxol, and the effects of dichloroacetate (DCA) on glucose metabolism. Methods: CCK-8 method was used to detect the drug resistance of paclitaxel in A549 and A549 / taxol cells. The production of CO2 and the formation of lipids after 14C-glucose uptake by A549 and A549 / taxol cells were detected by liquid scintillator. In addition, the uptake of 18F-2-deoxy-β-D-glucose (18F-FDG) and lactate production were measured using a gamma counter and a lactic acid assay kit, respectively. Results: The amount of CO2 release, the uptake of 18F-FDG and the amount of lactic acid production in A549 / taxol cells after 6-14C-glucose uptake were lower than those in A549 cells. The level of CO 2 released by 6-14 C-glucose in A549 cells after DCA treatment was increased, while the amount of CO 2 released by 6-14 C-glucose in A549 / taxol cells after DCA treatment did not change. CONCLUSION: A549 / taxol cells have certain mitochondrial oxidative respiration inhibition. DCA can promote oxidative respiration of mitochondria of A549 cells, but not of oxidative respiration of A549 / taxol cells.