人参皂苷Rg1对鼻咽癌CNE-2细胞凋亡、侵袭和迁移的影响

The Effects of Ginsenoside Rg1 on Apoptosis,Invasion and Migration of Human Nasopharyngeal Carcinoma CNE-2 cells

目的探究人参皂苷Rg1对鼻咽癌CNE-2细胞凋亡、侵袭和迁移的影响。方法采用不同浓度的人参皂苷Rg1处理鼻咽癌CNE-2细胞,同时选择无显著细胞毒性的Rg1低浓度、中浓度、高浓度(观察组)进行后续实验,对照组不做Rg1处理。采用CCK-8检测细胞增殖倍数,使用流式细胞术检测细胞凋亡情况,Transwell实验检测细胞侵袭能力,划痕实验检测细胞迁移能力,免疫印迹法检测相关蛋白表达情况。结果与对照组比较,观察组人参皂苷Rg1浓度越高,CNE-2细胞数量越少,增殖倍数、侵袭能力及Ki-67、血管内皮生长因子的表达水平越低,Q2区凋亡细胞越多,Caspase-3蛋白表达水平越高,差异有统计学意义(P <0. 01)。划线24 h后,观察组的缝隙间距明显大于对照组,差异有统计学意义(P <0. 01)。结论人参皂苷Rg1可促进鼻咽癌CNE-2细胞凋亡,抑制CNE-2细胞增殖、迁移和侵袭能力,为临床治疗鼻咽癌提供新思路和理论基础。

Objective The present study was designed to study the effect of ginsenoside Rg1on apoptosis,invasion and migration of human nasopharyngeal carcinoma CNE-2cells.Methods CNE-2cells were treated with different concentrations of ginsenoside Rg1.In the meantime,three groups(observation group)with low,medium and high Rg1without significant cytotoxicity were selected for subsequent experiments,while the control group was not treated with Rg1.Cell proliferation was detected by CCK-8assay,and cell apoptosis was detected by flow cytometry.Cell invasion was detected by transwell assays,cell migration was detected by wound-healing assay,and related protein expression was was detected by western blot.Results Compared with control group,ginsenoside Rg1inhibited the cell proliferation,migration and invasion ability of CNE-2cells in observation group,as evidenced by reduced number of CNE-2cells,decreased expression of Ki-67and vascular endothelial growth factor(VEGF)as well as increased cell numbers in Q2area and increased expression of Caspase-3in the observation group,and the difference was statistically significant(P<0.01).After streaking for24h,the gap spacing of the observation group was significantly greater than that of the control group,and there were significant differences(P<0.01).Conclusion Ginsenoside Rg1promoted apoptosis of human nasopharyngeal carcinoma CNE-2cells,and inhibited proliferation,migration and invasion of CNE-2cells,which might provide new insight and theoretical basis for the treatment of nasopharyngeal carcinoma.