%0 Journal Article
%T 极低频电磁场诱导人骨肉瘤细胞凋亡及其机制研究
%A 杨敏丽
%A 叶招明
%J 浙江大学学报(医学版)
%D 2015
%R 10.3785/j.issn.1008-9292.2015.05.13
%X 目的:探索极低频电磁场对人骨肉瘤细胞增殖凋亡的影响及其分子机制。方法:采用50 Hz、1 mT的极低频电磁场作用于人骨肉瘤细胞MG-63,通过MTT法检测MG-63细胞的存活率,通过流式细胞术检测MG-63细胞的凋亡率及活性氧水平,并检测MG-63细胞给予活性氧抑制剂N-乙酰半胱氨酸(NAC)及p38MAPK抑制剂SB203580作用后细胞凋亡率的变化;通过蛋白质印迹法检测极低频电磁场处理及NAC干预后MG-63细胞p38MAPK蛋白水平。结果:极低频电磁场能够显著抑制MG-63细胞的存活率,诱导MG-63细胞凋亡及活性氧生成;给予2.5 mmol/L NAC或SB203580干预后MG-63细胞凋亡率显著下降;极低频电磁场处理MG-63细胞后胞内p38MAPK表达增多,而NAC干预后磷酸化p38MAPK减少。结论:极低频电磁场可诱导人骨肉瘤细胞MG-63凋亡,其机制可能与活性氧生成增加、p38MAPK激活有关。</br>Abstract: Objective: To investigate the effects of extremely low frequency electromagnetic field (ELF-EMF) on human osteosarcoma cells and its mechanisms.Methods: Human osteosarcoma MG-63 cells were exposed to 50 Hz,1 mT ELF-EMF for 1, 2 and 3 h in vitro, with or without pretreatment by reactive oxygen species (ROS) inhibitor N acetylcysteine (NAC) or p38MAPK inhibitor SB203580. The proliferation of MG-63 cells was determined by MTT method; the apoptosis rate and ROS level in MG-63 cells were detected by flow cytometry. The expression of p38MAPK in MG-63 cells was determined by Western blotting.Results: ELF-EMF decreased the viability of MG-63 cells, inhibited cell growth, induced cell apoptosis and increased the level of ROS significantly. The apoptosis rate declined significantly after treatment with ROS inhibitor NAC or p38MAPK inhibitor SB203580. After exposure to ELF-EMF, p38MAPK in MG-63 cells was activated, and the phosphorylation level was also inhibited after treatment with NAC. Conclusion: ELF-EMF can induce the apoptosis of MG-63 cells. Increased ROS and p38MAPK activation may be involved in the mechanism. Key words: Electromagnetic fields Apoptosis/radiation effects Radiation injuries Osteosarcoma/pathology Cell line, tumor/radiation effects p38 Mitogen-activated protein kinases Reactive oxygen species
%K Electromagnetic fields Apoptosis/radiation effects Radiation injuries Osteosarcoma/pathology Cell line
%K tumor/radiation effects p38 Mitogen-activated protein kinases Reactive oxygen species
%U http://www.zjujournals.com/med/CN/10.3785/j.issn.1008-9292.2015.05.13