澳洲茄边碱通过Caspase3蛋白诱导人肺腺癌A549细胞的凋亡作用

运用中药龙葵提取物澳洲茄边碱处理人肺腺癌A549细胞,研究其对A549细胞的抑制及凋亡作用,探讨澳洲茄边碱对肺腺癌的作用机制。通过细胞增殖抑制实验检测不同浓度澳洲茄边碱对A549细胞增殖的影响,采用蛋白印迹法(Western blot)检测凋亡蛋白Caspase3的表达水平,采用流式细胞术测定处理后A549细胞的凋亡水平及细胞周期变化。结果显示,不同浓度澳洲茄边碱均能抑制A549的增殖,呈浓度效应;用不同浓度澳洲茄边碱处理A549细胞24h后,Western blot结果显示,随药物浓度增大,凋亡蛋白Caspase3水解程度增高,对A549凋亡作用明显增强;流式细胞术检测细胞凋亡的结果显示,20μmol·L-1澳洲茄边碱处理A549细胞后,细胞发生明显凋亡,其中早期凋亡细胞比例为25.35%,晚期凋亡细胞比例为11.47%;流式细胞术检测细胞周期的结果显示,20μmol·L-1澳洲茄边碱处理A549细胞后,细胞周期阻滞于G2/M期。本研究结果表明,澳洲茄边碱通过激活细胞凋亡通路中的Caspase3蛋白触发细胞凋亡,同时将A549细胞阻滞在细胞周期的G2/M期,抑制人肺腺癌细胞A549的生长。

Apoptosis of Human Lung Adenocarcinoma A549 Cells Induced by Solamangine through Activation of Caspase3 Protein

To explore the mechanism of solamangine extracted fromSolanum nigrum L.on human lung adenocarcinoma,A549 cells were treated by solamangine,and the growth inhibition,cell cycle,apoptosis as well as Caspase3 expression of the treated cell were analyzed.The results indicated that solamangine could dramatically inhibit the proliferation of A549 cells,and the inhibition and the activation of Caspase3 increased while the concentration of solamangine increased.The flow cytometry results showed that apotosis happened after 24 htreatment of solamangine,and the early and late apoptotic rates were 25.35% and 11.47%,respectively.The cell cycle was blocked at G2/M stage after treated with solamangine.This study revealed that solamangine triggered apotosis of A549 cells by activation of Caspase3,and blocked the cell cycle at G2/M stage,which then inhibited the proliferation of A549 cells.