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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。
Aim To investigate the effect and molecular mechanism of lanthanum chloride (LaCl3) on inducing human cervical carcinoma cell apoptosis in vitro and to provide a theoretical basis for exploring the medicinal value of rare earth compounds. Methods Morphological observation and MTT assay were used to determine the inhibition rate of lanthanum chloride on HeLa cells. Flow cytometry was used to analyze cell cycle and apoptosis rate. Caspase-3 Changes in protein expression were measured by spectrophotometry. Results Morphological analysis and MTT showed that lanthanum chloride could inhibit HeLa cell growth and induce apoptosis (P <0.05), and the effect was significant. Cell cycle experiments show that lanthanum chloride can make most of the cells arrested in the G1 phase, and a certain concentration-dependent; Lanthanum chloride-induced apoptosis also in a dose-dependent manner, 5μmol / L dose, the cells began to witness With the increase of drug concentration, the apoptotic rate increased continuously. The difference between each concentration and the control group was statistically significant (P <0.01). Western blotting experiments showed that lanthanum chloride can also up-regulate the expression and activity of activated Caspase-3 protein in a concentration-dependent manner. Conclusion Lanthanum chloride can inhibit the proliferation of human cervical cancer HeLa cells and induce the apoptosis of HeLa cells by activating Caspase pathway.