大黄素对人肺癌A549细胞增殖、凋亡的影响及机制探讨

Effect of Emodin on Proliferation and Apoptosis of Human Lung Cancer A549 Cells and its Mechanism

研究大黄素对人肺癌A549细胞的药效及其诱导细胞凋亡的分子机制。通过MTT法检测大黄素对A549细胞的杀伤作用;通过Annexin V-FITC/PI双染和流式细胞术检测大黄素对A549细胞的凋亡作用;通过免疫印迹法检测细胞凋亡相关蛋白的表达量变化。大黄素对A549细胞具有良好的杀伤作用且呈浓度依赖性;荧光显微镜和流式细胞术检测发现大黄素能够诱导A549细胞的凋亡且呈时间依赖性;Western blot检测显示大黄素处理A549细胞后,p-AKT、Bcl-2的表达量明显减少,Bad和cleaved-caspase-3的表达水平明显增加。大黄素通过调控AKT信号传导途径诱导人肺癌A549细胞的凋亡。

To investigate the pharmacologic effect and apoptotic mechanism of emodin on human lung cancer A549 cells, the viabili- ty of A549 cells were measured by MTI＂ assay.The apoptotic effect of emodin on A549 cells was detected by Annexin V-FITC/PI double staining and flow cytometry.The related apoptotic protein expression level was determined by western hlotting.Emodin sup- pressed the proliferation of A549 cells in a dose-dependent manner.The Annexin V-FITC/PI double staining and flow cytometry re- sults showed that emodin could induce A549 cell apoptosis in a time-dependent manner.The western blotting results showed that e- modin could significantly down-regulate p-AKT, Bcl-2 protein expression levels while up-regulated the Bad and cleaved-caspase-3 expression levels in A549 cells.Emodin significantly inhibited the proliferation of human lung cancer A549 cells by inducing mito- chondrial-related apoptosis via AKT signaling pathway.