Objective: To investigate the effects of Curcumol on the malignant biological characteristics of acute myeloid leukemia (AML) cells and its molecular mechanism, and to provide theoretical and experimental evidence for the anti-leukemia treatment of traditional Chinese medicine.
Methods: After the AML cell lines HL-60 and KG-1 cells were treated different concentrations of with Curcumol. The proliferation activity of cells was detected by CCK-8 method, and the expression changes of apoptotic proteins and PI3K/AKT signaling pathway proteins were detected by Western blot. Real-time quantitative fluorescence polymerase chain reaction (RT-qPCR) was used to detect the expression of Caspase family mRNA.
Results: Curcumol could inhibit the proliferation and induce apoptosis of HL-60 and KG-1 cells, promote apoptosis by up-regulating the expression of Bax and down-regulating the expression of Bcl-2 protein (P <0.05). When Curcumol interferes with HL-60 and KG-1 cells, it can also induce programmed cell death of AML by inhibiting PI3K/AKT signaling pathway. In addition, after the intervention of Curcumol, the expression of Caspase 3, Caspase 6, Caspase 8 and Caspase 9 were up-regulated in HL-60 cells (P <0.05), the expression of Caspase 3, Caspase 8 and Caspase 9 were significantly up-regulated in KG- cells (P <0.01), while the expression of Caspase 6 was weakly affected (P <0.05), but low concentration of Curcumol (< 60 μg/ml) had no effect on the expression of Caspase 6 in KG-1 cells (P >0.05).
Conclusion: Curcumol may mediate the programmed death of AML cells by inhibiting the PI3K/AKT signaling pathway, affecting the expression of Bcl-2 family proteins, and promoting the activation of core members of Caspase family, so as to play an anti-leukemia role.
题目: 莪术醇通过PI3K/AKT信号通路介导急性髓系白血病细胞程序性死亡.
目的: 探讨莪术醇对急性髓系白血病（AML）细胞恶性生物学特性的影响及其分子机制，为传统中医药抗白血病治疗提供理论与实验依据。.
方法: 用不同浓度莪术醇作用于AML细胞株HL-60、KG-1细胞后，CCK-8法检测细胞增殖活力，Western blot检测凋亡蛋白和PI3K/AKT信号通路蛋白的表达变化，实时荧光定量聚合酶链式反应（RT-qPCR）检测Caspase家族mRNA的表达情况。.
结果: 莪术醇可抑制HL-60、KG-1细胞的增殖活性，并诱导细胞凋亡，其通过上调Bax蛋白表达并下调Bcl-2蛋白的表达以促进细胞凋亡（P <0.05）。当莪术醇干预HL-60、KG-1细胞后，其亦可通过抑制PI3K/AKT信号通路激活而诱导AML细胞的程序性死亡。此外，莪术醇干预后可上调HL-60细胞的Caspase 3、Caspase 6、Caspase 8以及Caspase 9的表达（P <0.05）， 可显著上调KG-1细胞的Caspase 3、Caspase 8和Caspase 9的表达（P <0.01），对Caspase 6的表达影响微弱（P <0.05），但低浓度（< 60 μg/ml）莪术醇对KG-1细胞Caspase 6的表达基本无影响（P >0.05）。.
结论: 莪术醇可能通过抑制PI3K/AKT信号通路的激活、影响Bcl-2家族蛋白表达以及促进Caspase家族核心成员活化等介导AML细胞程序性死亡，从而发挥抗白血病作用。.
Keywords: Curcumol; acute myeloid leukemia; programmed cell death; anticancer mechanism.