Akt活性抑制对苍耳亭抗非小细胞肺癌活性的促进作用

Blocking of Akt activation accelerated the anti-NSCLC bioactivity of Xanthatin

目的:研究抑制非小细胞肺癌(NSCLC)A549细胞内的Akt激活对苍耳提取物苍耳亭(Xanthatin)抗肿瘤活性的影响。方法:MTT实验检测苍耳亭对A549细胞的抑制能力;Western blot实验检测苍耳亭对Akt、m TOR激活水平的影响;采用Akt1 siRNA干扰及Akt特异性抑制剂MK-2206研究Akt信号阻断对苍耳亭抗肿瘤效果的影响。结果:苍耳亭(2.5μmol/L^40μmol/L)能够剂量依赖性抑制A549细胞的增殖,起效剂量为20μmol/L,24h的IC50值为14.52μmol/L;苍耳亭处理24h能够促进Akt、m TOR的磷酸化激活;采用Akt1 siRNA干扰或MK-2206(1μmol/L)阻断Akt通路后能够提高10μmol/L剂量的苍耳亭作用24h对A549细胞的抑制作用。结论:阻断Akt信号对于苍耳亭抗NSCLC效果的发挥具有促进意义。

Objective： To investigate the effection of blocking Akt activation in non-small cell lung cancer（ NSCLC） A549 cells on the anti-cancer activity of xanthatin,a sesquiterpene lactone isolated from herbal-xanthium strumarium L. Methods： MTT assay measured the inhibition of xanthatin on A549 cell viability; Akt,m TOR activation were examed through Western blot assay; RNAi transfection and Akt specific inhibitor-MK-2206 was adopted to investigate the influence on the anti-cancer activity of xanthatin by blocking Akt signaling. Results： Xanthatin（ 2. 5μmol/L ～ 40μmol/L） can dose-dependently inhibited the viability of A549 cells. Initial effective concentration was 20μmol/L. The IC50 in 24h was 14. 52 μmol / L; xanthatin treatment for 24 h may accelerate Akt,m TOR phosphorylated activation; Blocking Akt activation through Akt1 siRNA or MK-2206（ 1μmol / L） may enhance the inhibition of A549 cells treated with 10μmol / L xanthatin for 24 h. Conclusion： Blocking Akt signaling may accelerate the anti-cancer activity of xanthatin on NSCLC.