牛蒡子苷元对体外C6胶质瘤细胞的抑制效果和凋亡机制

Research on Arctigenin in Proliferation and Apoptosis of C6 Glioma Cells

目的:探讨牛蒡子苷元对体外C6胶质瘤细胞的抑制效果和凋亡机制。方法:将牛蒡子苷元作用于C6胶质瘤细胞,采用CCK-8法测定各组细胞的生长抑制率;流式细胞术检测细胞凋亡情况;酶联免疫吸附试验检测TNF-α、IL-2的水平;Western blot检测Bax、Bcl-2、NF-кB蛋白表达水平。结果:与空白组比较,牛蒡子苷元组(2.5～40μmol/L)显著抑制C6胶质瘤细胞生长,诱导肿瘤细胞凋亡,其诱导效应具有浓度依赖性;牛蒡子苷元处理后,细胞中TNF-α、IL-2水平增加;牛蒡子苷元可以显著上调Bax蛋白表达,下调Bcl-2、NF-кb蛋白表达。结论:牛蒡子苷元可以促进C6胶质瘤细胞凋亡,可能是通过增强TNF-α、IL-2水平及上调Bax蛋白、下调Bcl-2、NF-кB蛋白水平而诱导肿瘤细胞凋亡。

Objective： To investigate the inhibitory effect and apoptosis mechanism of arctigenin on C6 glioma cells. Methods： Arctigenin acted on C6 glioma cells. CCK-8 was used to detect the growth inhibition rate of each group; flow cytometry was used to detect apoptosis rate of different group; the levels of TNF-α and IL-2 were detected by ELISA; the expressions of Bax, Bcl-2 and NF-кb proteins were analyzed by Western blot. Results： Compared with the blank group, arctigenin （2.5～40 μmol/L） significantly inhibited the growth of C6 glioma cells and induced apoptosis of tumor cells in concentration-dependent; after treatment with arctigenin, the levels of TNF-α and IL-2 in the cells were increased; arctigenin could up-regulate the expression of Bax protein and down-regulate the expression of Bcl-2 and NF-кb Proteins. Conclusion： Arctigenin can promote the apoptosis of C6 glioma cells, which maybe through enhance the levels of TNF-α, IL-2 and up-regulated Bax protein, down-regulate Bcl-2 and NF-кb proteins levels.