中文摘要：

目的:探讨淫羊藿素（icrm)通过PI3K/AKT信号通路对非小细胞肺癌H460细胞增殖的影响。方法:采用MTT比色实验检测，不同浓度(0、5、10、20、40、80Jma/L)淫羊藿素处理H460细胞24、48、72h后细胞增殖抑制率，流式细胞仪检测不同浓度淫羊藿素对H460细胞凋亡的影响,Wetenblot实验检测不同浓度淫羊藿素对H460细胞中PI3K、AKT、p-AKT、Cleavd-Caspase-9蛋白质表达水平的影响。结果:淫羊藿素可抑制非小细胞肺癌H460细胞的增殖,并表现为剂量和时间依赖性（P<0.05)。0、5、10、20jmol/L淫羊藿素处理只460细胞2411后，只460细胞凋亡率分别为（4.90±1.20)%、（13.5±2.32)%、（16.47±1.90)%和(27.43±3.15)%'<0.05。淫羊藿素可下调？13民、人『1'的表达水平,降低人『1'的磷酸化^-人『1')水平，上调Clavd-Capae-9表达水平(P<0.05)。结论:淫羊藿素可能通过抑制TOKAKT信号通路激活，抑制H460细胞增殖。

英文摘要：

Objective: To explore the effect of icaritin on non - small cell lung cancer H460 cell by the PI3K/AKTsignaling pathway. Methods:The H460 cells were treated with different concengtrations of icaritin ( 0 , 5 , 10,2 0 ,4 0 ,S/iJim ol/I,). The MTT assay was used to measure the proliferation inhibition rates at 24 ,48 ,72h in different concentrationsof icaritin. The Western blot was used to measure the protein levels of PI3K,AKT, p - AKT, Cleaved -Caspase - 9 in different concentrations of icaritin in the H460 cells. Results : Icaritin inhbition rates in d o s e - and tim e-d ep en d en t manner ( P < 0. 05 ) . 0 ,5 , 10 and 2 0 jm o l/L ic a ritin treated H 460cells for 24 h , the cell apotosis rates were (4 .9 0 ± 1 .2 0 ) % ,(13.5 ± 2 . 3 2 ) % ,(16. 47 ± 1 .9 0 ) % and (27. 43 ±3. 15) % ,P <0. 05. Icaritin could down - regulate PI3K,AKT and decrease the phosporlation of AKT,and up - regulateCleaved - Caspase - 9 ( P <0. 0 5 ). Conclusion:Icaritin can inhibit the proliferation of H460 cell possibly by inhibitingthe activation of PI3K/AKT signaling pathway.