二吲哚吡啶基吡咯烷对肺癌A549细胞增殖的影响

Effects of diindoline pyridinyl pyrrolidine on proliferation of A549 cells in lung cancer

目的:探讨二吲哚吡啶基吡咯烷(DIPRD)对肺癌A549细胞增殖的影响。方法:获取肺癌A549细胞,分别予以不同浓度(0、6.25、12.5、25、50、100μg/mL)的DIPRD孵育,孵育24 h后,分别采用细胞计数(CCK-8)检测细胞活性,克隆形成实验检测细胞增殖,免疫蛋白印迹实验(WB)检测蛋白激酶B(Akt)、雷帕霉素机械靶蛋白(mTOR)、细胞外调节蛋白激酶(Erk)蛋白磷酸化水平。结果:25μg/mL及以上浓度的二吲哚吡啶基吡咯烷孵育后可明显抑制A549细胞活力和细胞增殖。25μg/mL及以上浓度的二吲哚吡啶基吡咯烷孵育后可明显下调p-Akt、p-mTOR、p-Erk表达。结论:DIPRD可以有效抑制肺癌A549细胞增殖,此种作用分子机制可能与抑制Akt、mTOR及Erk蛋白磷酸化水平存在关系。

Objective:To investigate the effect of DIPRD on cell proliferation of A549 lung cancer cells.Method:Lung cancer A549 cells were obtained for cell culture,and incubated with DIPRD at different concentrations(0,6.25,12.5,25,50,100μg/mL).After incubation for 24 h,cell activity was detected by cell counting(CCK-8),and cell proliferation was detected by clonal formation assay.Immunoblotting(WB)was used to detect the phosphorylation levels of protein kinase B(Akt),mechanical target of rapamycin(mTOR)and extracellular regulatory protein kinase(Erk).Results:A549 cell viability and proliferation were significantly inhibited by incubation with diindoline pyridinyl pyrrolidine at 25μg/mL or above.The expression of p-Akt,p-mTOR and p-Erk was significantly down-regulated after incubation with diindoline pyridinyl pyrrolidine at 25μg/mL or above.Conclusion:DIPRD can effectively inhibit the proliferation of lung cancer A549 cells,and this molecular mechanism may be related to the inhibition of Akt,mTOR and Erk protein phosphorylation levels.