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To explore the inhibitory effect of dehydrocostus lactone on the proliferation of human chronic myeloid leukemia K562 cells and the underlying mechanisms.Cell viability was evaluated by CCK-8 assay. Flow cytometry was used to assess the effect of dehydrocostus lactone on the cell cycle and apoptosis of K562 cells. The levels of BCR/ABL-STATs-related molecules were analyzed by using Western blot.The CCK-8 assay showed that dehydrocostus lactone at graded concentration of 4, 6, 8, 10, 12 μmol/L could significantly inhibit the proliferation of K562 cells after exposure for 24 h. The proliferation inhibition rate was (24.32±3.05%), (42.91±3.89%), (46.35±4.93%), (77.06±5.42%) and (89.04±4.25%) respectively, showing statistically significantly different from (2.08±0.27%) in the control (P＜0.05). Also, the treatment with 5 and 10 μmol/L of dehydrocostus lactone induced K562 cell apoptosis, the apoptotic rate of K562 cells was significantly higher than that the control group (P＜0.05), and up-regulated the expression level of BAX and p21. Furthermore, dehydrocostus lactone (5 and 10 μmol/L) also increased the percentage of cells in G2/M [(8.53±1.71)% to (17.42±2.72) and (31.79±4.38%)](P＜0.05). The study results also revealed that dehydrocostus lactone significantly inhibited the expression of BCR/ABL STAT3, STAT5, CyclinB1, CDK1 and BCL-2, and up-regulated the expression level of BAX and p21.Dehydrocostus lactone can suppress the proliferation of K562 cells and induce the apoptosis of K562 cells through BCR/ABL-STAT signaling pathways.去氢木香内酯对K562增殖的抑制作用及其机制.探讨去氢木香内酯对慢性髓系白血病细胞系K562细胞的增殖抑制作用及其机制.应用CCK-8法检测细胞增殖抑制率，采用流式细胞术检测细胞凋亡和细胞周期，Western blot检测相关蛋白的表达.CCK-8检测结果显示，4、6、8、10、12 μmol/ L去氢木香内酯能够明显抑制K562细胞增殖，作用24 h抑制率分别为（24.32±3.05%）、（42.91±3.89%）、（46.35±4.93%）、（77.06±5.42%）、（89.04±4.25%），对照组为 （2.08±0.27%），差异有统计学意义（P＜0.05）；5、10 μmol/L去氢木香内酯能够诱导K562细胞凋亡，与对照组相比凋亡率由（2.73±0.46%）分别增加到（14.43±2.52%）、（31.71±3.58%）（P＜0.05）；去氢木香内酯能够使细胞周期阻滞在G2/M期，G2/M期细胞比例由（8.53±1.71%）分别增加到（17.42±2.72）、（31.79±4.38%）（P＜0.05）； 去氢木香内酯能够显著抑制BCL-2、CyclinB1、CDK1、BCR/ABL、STAT5、STAT3等的表达，上调BAX、p21的表达水平.去氢木香内酯通过BCR/ABL-STAT信号通路抑制K562细胞增殖，诱导K562细胞凋亡. |
