摘要
目的探讨氯化镧体外诱导人子宫颈癌细胞凋亡的作用和分子机制,为探索稀土化合物的药用价值提供理论依据。方法采用形态学观察、四甲基偶氮唑盐(MTT)比色法测定氯化镧对HeLa细胞的抑制率;流式细胞术分析细胞周期和细胞凋亡率,蛋白质印迹技术分析Caspase-3蛋白表达的改变,并以分光光度法测定其活性。结果形态学分析和MTT法显示氯化镧能够抑制HeLa细胞生长并诱导其凋亡(P<0.05),其作用呈明显的量效关系。细胞周期实验结果说明,氯化镧可令细胞大多阻滞于G1期,并呈一定的浓度依赖性;氯化镧诱导细胞凋亡亦有剂量依赖性,在5μmol/L剂量下,细胞开始凋亡,随着药物浓度的增加,凋亡率不断增高,各浓度与对照组相比差异都具有统计学意义(P<0.01)。蛋白质印迹实验显示氯化镧亦可上调活化的Caspase-3蛋白表达水平及活性且呈浓度依赖性。结论一定浓度的氯化镧可抑制人子宫颈癌HeLa细胞的增殖并通过激活Caspase途径诱导HeLa细胞凋亡。
Objective To explore apoptosis-inducing effect of lanthanum chloride in cervical cancer cells in vitro and the related mechanism,so as to provide a theoretical basis for medical use of rare earth complex.Methods The anti-tumor activity of lanthanum chloride against HeLa cells was examined by morphological observation and MTT（3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide） assay.Distribution of cell cycle and cell apoptosis were analyzed using flow cytometry（FCM）.The expression and activation of Caspase-3 were examined by Western blotting assay and spectrophotometry.Results Morphological observation and MTT assay showed that lanthanum chloride significantly induced apoptosis in HeLa cells and inhibited cell growth in a dose-dependent manner（P0.05）.FCM analysis showed that the cell ratio of G_0/G_1 phase increased and that of S phase decreased significantly with the increase of lanthanum chloride doses.Lanthanum treatment also induced cell apoptosis dose-dependently.The minimum dose of lanthanum chloride to trigger apoptosis was 5 μmol/L,and the apoptosis rate increased in a dose-dependent manner compared with the control group（P0.01）.Western blotting analysis showed that lanthanum chloride up-regulated Caspase-3 expression in a dose-dependent manner.Conclusion Lanthanum chloride can inhibit growth of human cervical cancer HeLa cells and induce cell apoptosis via Caspase pathway.
出处
《第二军医大学学报》
CAS
CSCD
北大核心
2011年第5期541-544,共4页
Academic Journal of Second Military Medical University
基金
国家自然科学基金(30960405)
江西省自然科学基金(2007GZY1132)~~
