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目的:探讨亚砷酸钠对人肺癌细胞株Spc-A1的抗癌机制。方法:用MTT法检测亚砷酸钠对Spc-A1细胞的增殖抑制作用;用Hoechst33258荧光染色法观察凋亡细胞的形态学改变;细胞凋亡率及相关蛋白Bcl-2和Fas的表达采用流式细胞仪测定。结果:亚砷酸钠对人肺癌细胞株Spc-A1的增殖具有一定程度的抑制作用。2μg/ml亚砷酸钠干预Spc-A1细胞12h、24h和48h后,在Hoechst荧光染色图片上可见细胞染色质浓缩及细胞核碎裂等典型的凋亡改变。给与1μg/ml、2μg/m l和4μg/ml亚砷酸钠作用Spc-A1细胞24h后,可以见到亚G1期凋亡峰,凋亡率随着药物浓度的增加明显增加。同时,流式细胞仪显示Bcl-2蛋白表达减少,而Fas蛋白表达增加。结论:亚砷酸钠对Spc-A1细胞的生长有明显的抑制作用,并可诱导细胞周期阻滞及细胞凋亡和坏死。Bcl-2的下调和Fas的上调可能是其中一种作用机制。
Objective: To investigate the anticancer mechanism of sodium arsenite on human lung cancer cell line Spc-A1. Methods: The inhibitory effect of sodium arsenite on the proliferation of Spc-A1 cells was detected by MTT assay. Morphological changes of apoptotic cells were observed by Hoechst 33258 staining. The apoptosis rate and the expression of Bcl-2 and Fas were detected by flow cytometry Cytometry. Results: Sodium arsenite inhibited the proliferation of human lung cancer cell line Spc-A1 to some extent. The changes of apoptosis in Spc-A1 cells induced by 2μg / ml sodium arsenite at 12h, 24h and 48h after Hoechst staining showed typical chromatin condensation and nuclear fragmentation. After treated with 1, 2 and 4 μg / ml sodium arsenite for 24 h, the apoptotic peak of sub-G1 phase was observed. The apoptosis rate of the cells increased with the increase of the drug concentration. Meanwhile, flow cytometry showed decreased Bcl-2 protein expression and increased Fas protein expression. Conclusion: Sodium arsenite has a significant inhibitory effect on the growth of Spc-A1 cells, and can induce cell cycle arrest and apoptosis and necrosis. Down-regulation of Bcl-2 and up-regulation of Fas may be one of the mechanisms.