The anti-tumor activity of dihydroartemisinin on glioma cells

目的 观察双氢青蒿素(DHA)对胶质瘤细胞增殖及凋亡的影响.方法 体外培养胶质瘤C6细胞,噻唑蓝(MTT)法检测DHA对C6细胞的增殖抑制作用;流式细胞仪分析测定细胞凋亡;Western blot检测Raf/丝裂原细胞外激酶(MEK)/细胞外信号调节蛋白激酶(ERK)信号通路及凋亡蛋白的表达.结果 DHA对C6细胞有明显抑制作用,在一定程度上呈剂量时间依赖性,DHA作用24、48 h后半数抑制剂量(IC50)分别为96.52、48.70 μmol/L;50、100 μmol/L DHA作用C6细胞10h后,其凋亡率分别为(10.32±0.63)％、(24.48 ±1.54)％,差异有统计学意义(P＜0.01);DHA可明显下调MEK和ERK蛋白磷酸化水平,抑制凋亡蛋白B细胞淋巴瘤/白血病-2(bcl-2)表达,而bcl-2相关X蛋白(bax)蛋白表达无明显变化.结论 DHA对C6细胞具有诱导凋亡和抑制增殖的 作用.Objective To investigate the effects of dihydroartiminisin (DHA) on the proliferation and apoptosis of glioma cells.Methods We examined the effects of DHA on the proliferation and apoptosis of glioma cell line C6 by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay and flow cytometry assay.The Raf/mitogen extracellular kinase (MEK)/extracelluar regulated protein kinase (ERK) signaling pathway and apoptotic protein changes were detected by Western blotting.Results The results showed that DHA effectively inhibited cell growth and induced apoptosis of C6 cells in a time-and dose-dependent manner.After incubation with DHA for 24 h and 48 h,the average 50％ inhibitory dose (IC50) was 96.52 μmol/L and 48.70 μmol/L,respectively.The cell apoptosis rate induced by 50 and 100 μmoL/L DHA for 10 h was (10.32 ± 0.63) ％ and (24.48 ± 1.54) ％,respectively.Western blotting results revealed that the phospho-MEK and phospho-ERK were downregulated.The expression level of anti-apoptotic proteins B cell lymphoma/leukemia-2 (bcl-2) was significantly reduced,but no changes were found in bcl-2 associated X protein (bax).Conclusion Our findings demonstrated that DHA inhibited proliferation and induced apoptosis of C6 glioma cells.中文核心期刊要目总览(PKU)中国科学引文数据库(CSCD)4767-7693