摘要
目的探讨九节龙皂苷对人脑胶质瘤细胞U373MG增殖的抑制作用及其机制。方法培养U373MG细胞系,随机分为二甲基亚砜对照组(control组)和九节龙皂苷治疗(ADS)组。采用甲基噻唑基四唑法检测不同剂量ADS对人胶质瘤细胞U373MG增殖的影响;流式细胞仪观察细胞凋亡情况。免疫组化检测凋亡蛋白Caspase-3、p-Caspase-3的表达变化。结果与对照组比较,ADS可显著降低U373MG细胞的生存率;流式细胞仪检测结果显示,随着ADS浓度的增大,U373MG细胞的凋亡率明显上升,免疫组化结果同样证明,ADS可呈剂量依赖性的促进凋亡信号Caspase-3和p-Caspase-3的高表达,不同组间差异有统计学意义(P<0.05)。结论 ADS可呈剂量依赖性的抑制U373MG细胞增殖,可能通过促进Caspase-3、p-Caspase-3的表达,诱发U373MG细胞大量凋亡,发挥重要的抗肿瘤作用。
Objective To study the effect of the ardipusilloside （ADS） on proliferation of the human glioma U373MG cells and its mechanism. Methods The cultured U373MG cells were randomly divided into two groups： dimethyl sulphoxide control group （control group ） and ADS treatment group （ADS group ）. MTT assay was performed to measure the effect of the different concentrations of ADS on the proliferation of U373MG cells. The apoptnsis of U373MG cells was detected by flowcytometry. The Caspase-3 and p-Caspase-3 were determined by immunocytochemistry, Results ADS significantly inhibited the viability of U373MG cells in a dose-and time- dependent manner. Flow cytometry results showed that U373MG cell apoptosis rate was significantly increased with the increase of concentration and incubation time , the imnamocytochemical results showed that Caspase-3 and p- Caspase-3 were highly expressed in U373MG cells after the treatment with ADS （P 〈 0. 05）. Conclusion ADS can inhibit the proliferation of U373MG cells and effectively induce the apoptosis of U373MG cells according to the activation of Caspase-3 and p-Caspase-3.
出处
《中华神经外科疾病研究杂志》
CAS
2013年第4期310-313,共4页
Chinese Journal of Neurosurgical Disease Research
基金
国家自然科学基金资助项目(30973623)
陕西省资源主导型产业关键技术(链)基金资助项目(2011KTCL03-01)
西京医院学科助推计划基金资助项目(XJZT12T05)
第四军医大学优秀文职人员培养基金(00002859)
