Vitexicarpin诱导肺癌A549细胞凋亡和对细胞周期作用的研究

Effect of Vitexicarpin on A549 Cell Cycle and Apoptosis

目的:研究蔓荆子黄素(Vitexicarpin)对人肺癌细胞株A549细胞增殖和凋亡的影响及其机制。方法:设计长春新碱(Vincristine)阳性对照组和空白阴性对照组及不同浓度的Vitexicarpin溶液作用于A549细胞,应用细胞增殖抑制试验和流式细胞仪检测技术,观察Vitexicarpin对A549细胞增殖的影响,以及其诱导A549细胞在不同时段的凋亡情况和对细胞周期的影响。结果:Vitexicarpin浓度为10μmol/L时对A549细胞的增殖抑制率超过50%,IC50为8.21μmol/L。另外,Vitexicarpin能有效诱导A549细胞凋亡。从Vitexicarpin作用4h开始,细胞被阻滞于G2/M期。随时间增加,G1/S期细胞逐渐减少,G2/M期细胞逐渐增多,且凋亡细胞逐渐增多。结论:Vitexicarpin能抑制A549细胞增殖,诱导A549细胞发生凋亡,将细胞阻滞于G2/M期是其可能作用机制。

Objective： To study the effect of vitexicarpin on the cell cycle and apoptosis of human lung cancer cell line A549. Methods： A549 cells were treated with vitexicarpin and vincristine solutions at various dosages. The effect of vitexicarpin on cell proliferation was assessed by MTT while the cell cycle and apoptosis were observed with flow cytometry. Results： The proliferation of A549 cells was inhibited by vitexicarpin. The rate of inhibition was more than 50% when the dose was 10 μmol/L. IC50 was 8.21μmol/L. Apoptosis in A549 cells was induced by vitexicarpin. At 4 hours after treatment, cells were blocked in G2/M. As time went on, the number of cells in G1/S was decreased, the number of cells in G2/M was increased, and the number of cells undergoing apoptosis was increased. Conclusion： Vitexicarpin inhibits proliferation and induces apoptosis in A549 cells. The probable mechanism involves blocking cells in G2/M.