五味子甲素对脑胶质瘤C6细胞生长的抑制作用及其机制

目的：探讨五味子甲素对脑胶质瘤C6细胞生长的抑制作用，阐明其作用机制。方法：培养大鼠脑胶质瘤C6细胞，将其分为对照组及50、100和200mg·L^-1五味子甲素组，采用MTT法检测C6细胞增殖率，流式细胞术分析细胞周期百分率，酶联免疫吸附实验（ELISA）检测细胞培养上清中CyclinD1、Bax、Bcl-2和Casepase-3蛋白表达水平。结果：与对照组比较，24和48h时50、100和200 mg·L^-1五味子甲素组细胞增殖率均明显降低（P < 0.01），72h时100和200 mg·L^-1五味子甲素组细胞增殖率明显降低（P < 0.05或P < 0.01）。与对照组比较，200 mg·L^-1五味子甲素组SubG₁期细胞百分率升高（P < 0.05），S期细胞百分率降低（P < 0.05）。与对照组比较，100和200mg·L^-1五味子甲素组细胞CyclinD1蛋白表达水平降低（P < 0.01），不同浓度五味子甲素组Bax蛋白表达水平升高（P < 0.05或P < 0.01），200mg·L^-1五味子甲素组Bcl-2蛋白表达水平降低（P < 0.01），不同浓度五味子甲素组Bax/Bcl-2比值明显升高（P < 0.01），200 mg·L^-1五味子甲素组Caspase-3蛋白表达水平升高（P < 0.01）。结论：五味子甲素通过下调CyclinD1蛋白表达水平、上调促凋亡因子Bax和Bcl-2表达水平而抑制C6细胞的生长。

Inhibitory effect of deoxyschizandrin on growth of brain glioma cells and its mechanism

Objective:To study the inhibitory effect of deoxyschizandrin on the growth of brain glioma C6 cells, and to explore its mechanism.Methods:The rat glioma C6 cells were cultured and divided into control group,50, 100,and 200 mg·L-1 deoxyschizandrin groups.The proliferation rates of C6 cells were examined by MTT assay;the changes of cell cycles were examined by flow cytometry;the expression levels of CyclinD1,Bax,Bcl-2 and Caspase-3 proteins in supernant were detected by ELISA assay. Results:Compared with control group, the proliferation rates at 24 and 48 h in 50,100,and 200 mg·L-1 deoxyschizandrin groups were significantly decreased (P <0.01),and the proliferation rates at 72 h in 100 and 200 mg·L-1 deoxyschizandrin groups were significantly decreased (P < 0.05 or P < 0.01 ). Compared with control group, the percentage of cells at SubG1 phase in 200 mg·L-1 deoxyschizandrin group was increased (P < 0.05 ), and the percentage of cells at S phase was decreased (P <0.05).Compared with control group,the expression levels of CyclinD1 in 100 and 200 mg· L-1 deoxyschizandrin groups were decreased (P < 0.01 );the expression levels of Bax protein in deoxyschizandrin groups were increased (P < 0.05 or P < 0.01 ), and the expression level of Bcl-2 protein in 200 mg · L-1 deoxyschizandrin group was decreased (P < 0.01 ), and the Bax/Bcl-2 value in deoxyschizandrin groups were increased (P < 0.01 ); the expression level of Caspase-3 protein in 200 mg · L-1 deoxyschizandrin group was increased (P < 0.01 ).Conclusion:Deoxyschizandrin could inhibit the growth of glioma cells through down-regulating the expression levels of CyclinD1 protein and up-regulating the expression levels apoptotic factors Bax and Bcl-2.