淫羊藿素通过PI3K/AKT信号通路抑制非小细胞肺癌H460细胞增殖

目的:探讨淫羊藿素（icaritin）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、80μmol/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，Western blot实验检测不同浓度淫羊藿素对H460细胞中PI3K、AKT、p-AKT、Cleaved-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、20μmol/L淫羊藿素处理H460细胞24h后，H460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）%，P＜0.05。淫羊藿素可下调PI3K、AKT的表达水平，降低AKT的磷酸化(p-AKT)水平，上调Cleaved-Caspase-9表达水平(P＜0.05)。结论:淫羊藿素可能通过抑制PI3K/AKT信号通路激活，抑制H460细胞增殖。

Icaritin inhibits the proliferation of non - small cell lung cancer H460 cells throug PI3K/AKT signaling pathway

Objective:To explore the effect of icaritin on non - small cell lung cancer H460 cell by the PI3K/ AKT signaling pathway. Methods:The H460 cells were treated with different concengtrations of icaritin(0,5,10,20,40, 80μmol/ L). The MTT assay was used to measure the proliferation inhibition rates at 24,48,72h in different concen-trations of 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 could increase the proliferation inhbition rates in dose - and time - dependent manner(P < 0. 05). 0,5,10 and 20μmol/ L icaritin treated H460 cells for 24 h,the cell apotosis rates were(4. 90 ± 1. 20)% ,(13. 5 ± 2. 32)% ,(16. 47 ± 1. 90)% and(27. 43 ± 3. 15)% ,P < 0. 05. Icaritin could down - regulate PI3K,AKT and decrease the phosporylation of AKT,and up - regu-late Cleaved - Caspase - 9(P < 0. 05). Conclusion:Icaritin can inhibit the proliferation of H460 cell possibly by in-hibiting the activation of PI3K/ AKT signaling pathway.