目的初步研究不同浓度的柴胡皂苷A(saikosaponin A,SSA)对鼻咽癌细胞凋亡诱导作用及其机制。方法体外常规培养人鼻咽癌5-8F细胞,将SSA溶解于含0.2%二甲基亚砜(dimethyl sulfoxide,DMSO)的Dulbecco改良Eagle培养基(dulbecco''s modified eagle medium,DMEM)高糖培养基中,分别以0(对照组)、5、10和20μmol/L SSA作用于鼻咽癌细胞48小时,之后用免疫印迹法检测不同浓度的SSA对鼻咽癌细胞总的细胞外调节蛋白激酶(total extrallular signal regulated protein kinase,t-ERK)及磷酸化的细胞外调节蛋白激酶(phosphorylated extrallular signal regulated protein kinase,p-ERK)蛋白表达量的影响,并通过流式细胞仪检测细胞凋亡水平的变化。结果与对照组相比,10~20μmol/L SSA作用48小时,鼻咽癌细胞中ERK蛋白磷酸化水平明显降低,差异有统计学意义;而与对照组相比,10~20μmol/L SSA处理的鼻咽癌细胞凋亡细胞数明显增加,差异有统计学意义,且随着SSA浓度的增加,凋亡细胞数也相应增多。结论一定浓度的SSA可引起鼻咽癌细胞凋亡率的上升,其机制可能与抑制ERK蛋白磷酸化表达有关。
Objective To investigate the effects of saikosaponin A ( SSA) on p-ERK expressions and apoptosis in human nasopharyngeal carcinoma cell. Methods SH-SY5Y cells were established in vitro firstly, then SSA was dissolved in high glucose DMEM cultures which include 0. 2% DMSO, and the cul-tures were pretreated individually with 0 ~10 μmol/L SSA for 48 hours, and then, the expressions of t-ERK and p-ERK were analyzed by western-blotting in the cells for different concentrations of SSA. At the same time, apoptosis levels of cells were analyzed flow cytometry. Results A significant inhibition of p-ERK was observed in 5-8F cells after treatment with SSA from 10 ~20 μmol/L groups for 48 h. It also shows that SSA from 10~20 μmol/L groups could also induce the apoptosis of 5-8F cells. Conclusion These results demonstrate that SSA can promote the apoptosis of nasopharyngeal carcinoma cells, and the mechanism may be related to the inhibition of ERK active expression.