摘要
目的探讨紫花牡荆素(CAS)诱导人肺腺癌A549细胞凋亡及其机制。方法平皿集落法测定CAS对A549细胞生长的抑制作用;碘化丙啶(PI)染色流式细胞术(FCM)分析细胞凋亡率;丫啶橙/溴乙啶(AO/EB)荧光染色观察细胞凋亡形态;Western blot检测FoxM1(forkhead box protein M1)表达水平。结果 CAS能抑制人肺腺癌A549细胞生长,呈浓度依赖性,半数抑制浓度(IC50)值为7.26μmol L-1;CAS处理后A549细胞呈典型凋亡细胞形态学改变,诱导细胞凋亡呈浓度依赖性;CAS诱导A549细胞FoxM1蛋白表达下调,呈浓度和时间依赖性。结论 CAS抑制人肺腺癌A549细胞的生长并诱导其凋亡,其作用机制可能与FoxM1表达下调有关。
Objective To investigate the apoptosis of human lung adenocarcinoma cancer A549 cells induced by casticin （CAS） and the mechanism. Methods The inhibitory effect of CAS on the proliferation ofA549 cells was measured by agar colony formation assay. CAS-induced apoptosis rates ofA549 cells were observed by flow cytometry （FCM） with prop- idium iodide staining. The cell apoptosis morphology was observed by AO/EB fluorescence staining. FoxM1 expression was analyzed by Western blot. Results CAS had a significantly inhibitory effect on the cell proliferation in A549 cells in a concentration-dependent manner, and the 1C5o was 7.26 Ixmol ~ L - i. CAS treated A549 cells presented typical apoptotic morphology, and CAS induced the apoptosis ofA549 cells in a concentration-dependent manner. Western blot demonstrated that expression of FoxM1 was down-regulated in a concentration-time-dependent manner. Conclusion CAS can inhibit the proliferation ofA549 cells and induce the apoptosis ofA549 cells, which may be due to the down-regulation of FoxM1 expression.
出处
《中南药学》
CAS
2013年第9期644-648,共5页
Central South Pharmacy
基金
2012年度湖南省中医药科研计划项目(No.201269)
