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目的探讨秦皮甲素对肺癌细胞A549增殖、凋亡的影响及机制。方法人肺癌细胞A549分为对照组、阳性对照组(5-Fu 0.77 mmol/L)、秦皮甲素0.4、0.8、1.6 mmol/L组,四甲基偶氮噻唑蓝比色法检测肺癌细胞A549的增殖率,流式细胞仪检测细胞周期、细胞凋亡率和线粒体膜电位的变化,免疫印迹法检测Bax,Bcl-2,Caspase-3蛋白表达改变。结果秦皮甲素可抑制人肺癌细胞A549的增殖,IC50为0.4 mmol/L;降低线粒体膜电位并诱导凋亡;与对照组比较,人肺癌细胞A549经秦皮甲素1.6 mmol/L组处理后,S期细胞比例[(20.35±0.26)%]升高,G2/M期细胞比例[(25.46±0.17)%]降低;与对照组比较,秦皮甲素1.6 mmol/L组细胞凋亡率(29.15%)明显升高,Bax和Caspase-3蛋白表达增强,Bcl-2蛋白表达受到抑制,呈剂量-效应关系。结论秦皮甲素可以通过线粒体途径诱导人肺癌细胞A549凋亡。
Objective To investigate the effects of aesculin on the proliferation and apoptosis of lung cancer cell line A549 and its mechanism. Methods A549 lung cancer cells were divided into control group, positive control group (5-Fu 0.77 mmol / L), aesculin 0.4,0.8 and 1.6 mmol / L group, and MTT assay of lung cancer A549 The proliferation rate, the changes of cell cycle, apoptosis rate and mitochondrial membrane potential were detected by flow cytometry. The expressions of Bax, Bcl-2 and Caspase-3 were detected by Western blotting. Results Aesculin could inhibit the proliferation of human lung adenocarcinoma A549 cells with an IC50 of 0.4 mmol / L, reduce the mitochondrial membrane potential and induce apoptosis. Compared with the control group, A549 cells treated with arachidin 1.6 mmol / L, (20.35 ± 0.26)%] in S phase and decreased in G2 / M phase [(25.46 ± 0.17)%]. Compared with control group, the apoptosis rate of AEC in 1.6 mmol / L group was significantly higher than that in control group %) Was significantly increased, Bax and Caspase-3 protein expression increased, Bcl-2 protein expression was inhibited, the dose-response relationship. Conclusions Aesculin can induce apoptosis of A549 cells through mitochondrial pathway.