在我们大量前期研究工作的基础上，研究PI3K/AKT/NF-κB信号通路在丹参酮衍生物（丹参酮Ⅰ、ⅡA及隐丹参酮）抗白血病中的作用机制，并探讨其药物作用靶点。以不同类型的白血病细胞株、原代白血病细胞为研究对象，给予不同剂量的丹参酮衍生物、PI3K/AKT及NF-κB抑制剂（LY294002及SN50）单独或联合作用于白血病细胞，检测细胞增殖抑制率及凋亡率的变化。运用肿瘤信号通路基因芯片, 检测PI3K/AKT/NF-κB通路及Bcl-2、Caspase家族中与细胞增殖及凋亡相关调节基因的变化，通过Western blot进一步检测差异基因的表达水平, 阐明药物对白血病细胞的体外作用机制。本课题首次探讨了PI3K/AKT/NF-κB通路介导的丹参酮衍生物的体外抗白血病作用及其药物作用靶点，为临床白血病的辅助治疗提供了新的手段。

To investigate the role of PI3K/AKT/NF-κB signaling pathway and the molecular targets in Tanshinone (Tan) derivatives (Tanshinone Ⅰ，ⅡA and cryptotanshinone) caused antileukemia effects. In vitro antileukemia effect was observed in different types of leukemic cells, and all these leukemic cells were treated by different concentrations of Tan as well as inhibitors of PI3K/AKT and NF-κB（LY294002 and SN50）, cell proliferation and apoptosis ratio were also detected after the cells were treated by different concentrations of the above drugs. Gene chips of cancer cell signaling pathways were used to detect the variations of PI3K/AKT/NF-κB pathways as well as Bcl-2 and Caspase families, and western blot was also used to observe the variation of different gene expression before and after Tan treatment. The study will provide accurate molecular targets and strong laboratory evidence in Tan induced antileukemia effects.