探讨髓系白血病细胞株的糖酵解表型特征及其潜在的调控机制。葡萄糖试剂盒和乳酸试剂盒分别检测5株白血病细胞培养上清液中的葡萄糖消耗(G)和乳酸生成含量(L),计算L/G比值来评估糖酵解水平;定量PCR检测糖酵解相关基因GLUT、MCT1 mRNA表达;CCK8法检测细胞体外增殖能力;Western blot检测AKT蛋白磷酸化水平。结果显示,KG1a和K562细胞体外培养24 h后的L/G比值分别为1.78和1.71,接近糖酵解表型时L/G为2的比值,同时这两株细胞高表达糖酵解相关基因GLUT1和MCT1 mRNA。低糖(0.5 mmol/L)、中糖(5 mmol/L)、高糖(10 mmol/L)处理KG1a和K562细胞40 h后,两株细胞的增殖能力、葡萄糖消耗和乳酸生成随葡萄糖浓度增加而增强,高糖组增加更为显著(P<0.05)。相反,若糖酵解抑制剂2-DG(0,5,10 mmol/L)处理白血病细胞40 h后,两株细胞的增殖能力及糖酵解代谢水平随2-DG浓度增加而降低,高浓度2-DG组(10 mmol/L)降低更为显著(P<0.05)。此外,AKT抑制剂低浓度(5μmol/L)短时间(12 h)处理后能抑制白血病细胞AKT蛋白磷酸化水平,同时降低细胞的葡萄糖消耗和乳酸生成(P<0.05)。该研究提示髓系白血病细胞具有高糖酵解表型,AKT可能参与调控白血病的糖代谢过程,这有助于阐明白血病的能量代谢特征以及为白血病的靶向抗代谢治疗奠定基础。 To investigate the phenotype of glycolysis and its potential regulatory mechanism in myeloid leukemia cell lines. Glucose and lactate kit were used to detect the glucose consumption (G) and lactate production (L) in 5 leukemia cell culture supernatants, and the L / G ratio was calculated to evaluate the level of glycolysis; quantitative PCR was used to detect the glycolytic Related gene GLUT, MCT1 mRNA expression; CCK8 assay of cell proliferation in vitro; Western blot detection of AKT protein phosphorylation level. The results showed that the L / G ratios of KG1a and K562 cells cultured in vitro for 24 h were 1.78 and 1.71, respectively. The ratio of L / G to the glycolytic phenotype was 2, and the two cells highly expressed the genes related to glycolysis GLUT1 and MCT1 mRNA. The proliferative ability, glucose consumption and lactate production of KG1a and K562 cells were increased with the increase of glucose concentration at low glucose (0.5 mmol / L), medium sugar (5 mmol / L) and high glucose (10 mmol / L) Increased, high glucose group increased more significantly (P <0.05). On the contrary, if the leukemia cells were treated with 2-DG (0, 5, 10 mmol / L) for 2 hours, the proliferation and glycolysis metabolism of the two cells decreased with the increase of the concentration of 2-DG The concentration of 2-DG group (10 mmol / L) decreased more significantly (P <0.05). In addition, AKT inhibitor at a low concentration (5μmol / L) for a short time (12h) inhibited AKT phosphorylation and decreased glucose consumption and lactate production in leukemia cells (P <0.05). This study suggests that myeloid leukemia cells have a high glycolytic phenotype, and that AKT may be involved in the regulation of glucose metabolism in leukemias, which may help elucidate the energy metabolism characteristics of leukemia and lay a foundation for the targeted antimetabolites treatment of leukemia.