摘要
目的研究越桔原花青素诱导脑胶质瘤细胞凋亡的作用,探讨越桔原花青素诱导胶质瘤细胞凋亡的机制。方法培养人脑胶质瘤SHG-44细胞,四甲基偶氮唑蓝法检测越桔原花青素作用后SHG-44细胞的生长抑制率,倒置显微镜观察药物作用后细胞生长的变化;Annexin V/PI分析细胞凋亡率;细胞免疫组化法检测bax蛋白的表达;蛋白质印迹法检测bax、bcl-2和caspase 3蛋白的表达。结果 8、40和200μg·L-1越桔原花青素均明显抑制SHG-44细胞的生长,倒置显微镜下观察到细胞密度明显降低;各用药组的细胞凋亡率随着药物浓度升高而增高;各用药组细胞表达bax蛋白和caspase 3蛋白明显增加,表达bcl-2蛋白减少。结论越桔原花青素通过上调bax蛋白和下调bcl-2蛋白的表达,激活线粒体通路后促进肿瘤细胞凋亡并抑制肿瘤细胞生长。
OBJECTIVE To study the effects of Vaccinium vitis procyanidin on glioma SHG-44 cells and explore the mechanism of Vaccinium vitis procyanidin induced apoptosis. METHODS SHG-44 cells were cultured. The rates of inhibition were examined by MTT assay; and the density of SHG-44 cells was observed by inverted microscope; the expression of bax protein was detected by cytohistoimmunochemistry,bax,bcl-2 and caspase 3 proteins were examined by Western blot assay. RESULTS The rates of inhibition of SHG-44 cells were increased in 8,40 and 400 μg·L^-1 Vaccinium vitis procyanidin groups,and the density was decreased; the apoptotic rates were increased with dose increased; the expression of bax and caspase 3 proteins was increased in treated groups,but the expression of bcl-2 protein was decreased in treated groups. CONCLUSION Vaccinium vitis procyanidin could induce the apoptosis in glioma SHG-44 cells through up-regulating the expression of bax protein and down-regulating the expression of bcl-2 protein,and then activated the mitochondrial pathway.
出处
《中国药学杂志》
CAS
CSCD
北大核心
2015年第6期507-511,共5页
Chinese Pharmaceutical Journal
基金
吉林省教育厅资助项目(2013324)
吉林省卫生厅资助课题(2013Z203)
国家自然科学基金资助项目(81201671)
