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目的:探讨水飞蓟宾(silybin,SIL)对人食管癌EC109细胞系的作用,并探求Notch1以及凋亡通路在其中的角色。方法:实验分为对照组和SIL处理组(75、150、300μM),各组细胞分别处理12、24、36小时。Cell Counting Kit-8(CCK-8)测细胞活力;粘附实验测细胞粘附能力;Caspase-Glo誖3/7定量试剂盒测细胞Caspase3/7的表达;Western-blot测Notch1、Bcl2和Bax蛋白表达。结果:CCK-8检测结果示SIL可有效抑制EC109细胞的活力(P<0.01),并呈浓度时间依赖性;粘附实验结果示SIL可以降低EC109细胞粘附能力(P<0.01);Caspase3/7检测结果示SIL可以使EC109细胞Caspase3/7活性升高(P<0.01);Western-blot检测结果显示SIL可以使EC109细胞Notch1和Bcl2表达下降,Bax表达上升(P<0.01)。结论:SIL可有效抑制食管癌EC109细胞活力,其作用机制可能与抑制Notch1通路,激活凋亡通路相关,SIL可能是食管癌药物治疗领域具有开发前景的药物。
Objective: To investigate the effect of silybin (SIL) on human esophageal carcinoma cell line EC109 and investigate the roles of Notch1 and apoptosis pathway. Methods: The experiment was divided into control group and SIL treatment group (75,150,300μM). The cells in each group were treated for 12, 24 and 36 hours respectively. Cell viability was measured by Cell Counting Kit-8 (CCK-8); cell adhesion was measured by adhesion assay; Caspase3 / 7 expression was detected by Caspase-Glo assay against 3/7 kit; Western blot was used to detect Notch1, Bcl2 and Bax Protein. Results: The results of CCK-8 showed that SIL could effectively inhibit the viability of EC109 cells (P <0.01) in a time-and concentration-dependent manner. Adhesion experiments showed that SIL could reduce the adhesion of EC109 cells (P <0.01) The results of Western-blot showed that SIL could decrease the expression of Notch1 and Bcl2 and increase the expression of Bax in EC109 cells (P <0.01) .3. Conclusion: SIL can effectively inhibit the viability of esophageal carcinoma EC109 cells. The mechanism may be related to the inhibition of Notch1 pathway and activation of apoptotic pathway. SIL may be a promising drug in the field of esophageal cancer drug therapy.