中文摘要：

目的将在 HL-60 人的 myeloid 白血病房间在增长和 apoptosis 上与砷三氧化物(As2O3 ) 调查 carnosic 酸(CA ) 的 synergistic 效果，和细胞的发信号小径在这些效果包含了的专业。方法 HL-60 细胞的增长被 3-(4,5-dimethylthiazol-2-yl ) 测量 -2,5-diphenyltetrazolium 溴化物(MTT ) 分析。房间周期分发和 apoptosis 被流动 cytometry 监视。casepase-9 的激活，房间死亡的 Bcl-2-associated 收缩筋(坏) ， p 坏，在染色体十上删除的 p27，磷酸酶和 tensin 相当或相同的事物(PTEN ) ， Akt， p-Akt 被西方的污点分析估计。PTEN mRNA 的表示被反向的抄写聚合酶链反应(RT-PCR ) 测试分析。结果 CA 在一个剂量依赖者和时间依赖者举止减少了 HL-60 房间生存能力，并且导致了 G1 拘捕和 apoptosis。而且， CA upregulated PTEN 表示，堵住了表明小径，坏、重新激活的 caspase-9 的随后禁止的 phosphorylation，和 p27 的提高的层次的 Akt。CA 也扩充了 As2O3 的这些效果。结论 CA 可能是为白血病处理的联合治疗的一个新奇候选人；这些效果显然与表明小径的 PTEN/Akt 的调整被联系。

英文摘要：

Objective： To investigate the synergistic effects of carnosic acid （CA） with arsenic trioxide （As203） on proliferation and apoptosis in HL-60 human myeloid leukemia cells, and the major cellular signaling pathway involved in these effects. Methods： HL-60 cellular proliferation was measured by 3-（4,5-dimethylthiazol-2-yl）- 2,5-diphenyltetrazolium bromide （MTF） analysis. Cell cycle distribution and apoptosis were monitored by flow cytometry. The activation of casepase-9, Bcl-2-associated agonist of cell death （BAD）, p-BAD, p27, phosphatase and tensin homolog deleted on chromosome ten （PTEN）, Akt, p-Akt was assessed by Western blot analysis. The expression of PTEN mRNA was tested by reverse transcription polymerase chain reaction （RT-PCR） analysis. Results： CA reduced HL-60 cell viability in a dose- and time-dependent manner, and induced G1 arrest and apoptosis. Moreover, CA upregulated PTEN expression, blocked the Akt signaling pathway, subsequently inhibited phosphorylation of BAD, reactivated caspase-9, and elevated levels of p27. CA also augmented these effects of As203. Conclusion： CA might be a novel candidate of the combination therapy for leukemia treatment; these effects were apparently associated with the modulation of PTEN/Akt signaling pathway.