P53介导的活性氧通路对硒酸酯多糖诱导骨肉瘤细胞凋亡的作用

摘要

Objective To analyze the role of P53 mediated ROS pathway in Kappa-selenocarrageenan induced osteosarcoma tumor cell apoptosis. Methods Different concentrations selenocarrageenan were used to treat the OS-732 cells, the expression levels of pro-liferating cells, apoptosis, ROS level and apoptosis-related proteins in each group were analyzed. Results After selenocarrageenan pro-cessing, the OS-732 cell growth inhibition showed varying degrees with a time-and concentration-dependent manner, and 60 g/L concentration for 48 h was the maximum inhibition rate of OS-732;20, 40, 60 μg/mL after concentrations 24 h, ROS levels were sig-nificantly increased ( P < 0. 05 ) , OS-732 cell apoptosis was significantly increased, and the percentage of early apoptotic cells and late apoptotic cells were significantly different compared with 0 μg/mL ( P < 0. 05 );P53, Caspase-9 Bax expression increased with the in-crease of drug concentration, while the expression of Bcl-2 was significantly lowered ( P < 0. 05 ) . Conclusion Kappa-selenocar-rageenan can significantly inhibit OS-732 cell proliferation, induce apoptosis, and P53-mediated ROS pathway may play an important role.%目的 探讨P53介导的活性氧( ROS )通路在硒酸酯多糖诱导骨肉瘤细胞凋亡中的作用.方法 采用不同质量浓度硒酸酯多糖处理OS-732细胞,分析各组细胞的增殖、凋亡情况、ROS水平及凋亡相关蛋白的表达水平.结果 硒酸酯多糖处理后,OS-732细胞生长受到不同程度抑制,呈现出时间和浓度依赖性,60 g/L质量浓度处理48 h时OS-732细胞抑制率最高;20,40,60μg/mL质量浓度处理24 h后, ROS水平显著增加( P<0. 05),OS-732细胞凋亡率显著升高,其中早期凋亡细胞及晚期凋亡细胞百分比与0μg/mL相比均有显著性差异( P<0. 05);P53,Caspase-9及Bax表达随着药物质量浓度的增加而升高,而Bcl-2的表达显著降低( P<0. 05).结论 硒酸酯多糖处理骨肉瘤细胞能显著抑制OS-732细胞的增殖活性,促进凋亡,细胞内高水平的ROS状态可能在此过程中有重要作用.