Sheng Liang-He, Xu Meng, Xu Li-Qun, Xiong Fei
Zhong Yao Cai. 2014 May;37(5):840-3.
To evaluate the proliferation inhibitory effect of Lappaconitine (LAP) on non-small cell lung cancer cell line A549 cells in vitro and its possible mechanism.
A549 cell was cultured with different concentrations of LAP. Cellular proliferation was determined with MTT. Cell cycle and apoptosis were detected with FCM technology. The Cyclin E1 gene expression was checked by Real-time Quantitative PCR method.
LAP could inhibit the proliferation of A549 cells in vitro in a dose-dependent manner. LAP could induce apoptosis of A549 cell. Cell cycle was stopped at the G1 + G0 phase by LAP with FCM technology. With the increasement of LAP concentration, the ratio of G1 + G0 phase was increased and the ratio of S phase and G2 + M phase was decreased; The apoptotic rate was gradually increased, and the Cyclin E1 gene expression was down-regulated.
LAP has the inhibitory effect on the growth of A549 cells, which is related to the cell cycle arrest in G0/G1 phase, apoptosis and down-regulation of Cyclin E1 gene expression.
评价去甲乌药碱(LAP)对非小细胞肺癌细胞系A549细胞的体外增殖抑制作用及其可能机制。
用不同浓度的LAP培养A549细胞。采用MTT法测定细胞增殖。用流式细胞术检测细胞周期和凋亡。用实时定量PCR法检测细胞周期蛋白E1基因表达。
LAP能体外抑制A549细胞增殖,呈剂量依赖性。LAP能诱导A549细胞凋亡。流式细胞术显示LAP使细胞周期停滞于G1+G0期。随着LAP浓度增加,G1+G0期比例升高,S期和G2+M期比例降低;凋亡率逐渐升高,细胞周期蛋白E1基因表达下调。
LAP对A549细胞生长有抑制作用,这与细胞周期阻滞于G0/G1期、细胞凋亡及细胞周期蛋白E1基因表达下调有关。