白附子提取物对胶质瘤细胞的生长抑制作用及其机制

Inhibitory effect of Rhizoma typhonii extract on growth of glioma cells and its mechanism

目的:研究白附子提取物对体外培养的脑胶质瘤细胞生长的影响,初步探讨其抑制胶质瘤细胞生长的机制。方法:培养人脑胶质瘤SHG-44细胞,分为空白对照组和不同剂量(8、40、200和1 000μg·L-1)白附子提取物组,MTT法检测白附子提取物对SHG-44细胞生长的抑制作用,ELISA法检测细胞分泌Bax和caspase-3蛋白水平,Western blotting法检测细胞中caspase-3蛋白表达水平。结果:与空白对照组比较,24h时200和1 000μg·L-1白附子提取物组、48h时8、40、200和1 000μg·L-1白附子提取物组细胞的生长抑制率明显升高(P<0.05或P<0.01);48h时白附子提取物组细胞分泌Bax和caspase-3蛋白水平均呈上升趋势,40、200和1 000μg·L-1白附子提取物组与空白对照组比较差异均有统计学意义(P<0.05或P<0.01);不同剂量白附子提取物组SHG-44细胞caspase-3蛋白表达水平随白附子提取物剂量的增加呈上升趋势,与空白对照组比较差异均有统计学意义(P<0.01)。结论:白附子提取物通过上调Bax蛋白表达水平,使caspase-3表达水平增加,激活凋亡通路,抑制细胞生长。

Objective To study the influence of Rhizoma typhonii extract on the growth of glioma SHG-44 cells cultured in vitro,and to explore the mechanism of the inhibitory effect of Rhizoma typhonii extract on the growth of glioma cells.Methods The SHG-44 cells were cultured and divided into blank control group and 8,40,200,1 000μg·L-1 Rhizoma typhonii extract groups.The inhibitory effect of Rhizoma typhonii extract on the growth of glioma SHG-44 cells was measured by MTT assay.The secretion levels of Bax and caspase-3 proteins were examined by ELISA assay.The expression level of caspase-3protein was examined by Western blotting method.Results Compared with blank control group,the inhibitory rates of the growth of SHG-44 cells in 200,1 000μg·L-1 Rhizoma typhonii extract groups at 24h,and 8,40,200,and 1 000μg·L-1 Rhizoma typhonii extract groups at 48h were significantly increased（P〈0.05or P〈0.01）.The secretion levels of Bax and caspase-3proteins in 40,200,and 1 000μg·L^-1 Rhizoma typhonii extract groups at 48h were increased compared with blank control group（P〈0.05or P〈0.01）.Compared with blank control group,the expression levels of caspase-3 protein in different doses of Rhizoma typhonii extract groups were increased significantly（P〈0.01）.Conclusion Rhizoma Typhonii extract can inhibit the growth of cells through up-regulating the expression of Bax protein,increasing the expression level of caspase-3 protein and activating apoptosis pathway.