CAJ | 학술논문

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.
목적 탐토P53개도적활성양( ROS )통로재서산지다당유도골육류세포조망중적작용.방법 채용불동질량농도서산지다당처리OS-732세포,분석각조세포적증식、조망정황、ROS수평급조망상관단백적표체수평.결과 서산지다당처리후,OS-732세포생장수도불동정도억제,정현출시간화농도의뢰성,60 g/L질량농도처리48 h시OS-732세포억제솔최고;20,40,60μg/mL질량농도처리24 h후, ROS수평현저증가( P<0. 05),OS-732세포조망솔현저승고,기중조기조망세포급만기조망세포백분비여0μg/mL상비균유현저성차이( P<0. 05);P53,Caspase-9급Bax표체수착약물질량농도적증가이승고,이Bcl-2적표체현저강저( P<0. 05).결론 서산지다당처리골육류세포능현저억제OS-732세포적증식활성,촉진조망,세포내고수평적ROS상태가능재차과정중유중요작용.
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.