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藏红花素诱导人脑胶质瘤细胞U87凋亡的作用机制研究
引用本文:边寰,张磊,王蓉,校鑫,李娟,王西玲,费舟.藏红花素诱导人脑胶质瘤细胞U87凋亡的作用机制研究[J].中国医药导报,2013(27):11-13.
作者姓名:边寰  张磊  王蓉  校鑫  李娟  王西玲  费舟
作者单位:[1]第四军医大学学员旅三队,陕西西安710032 [2]第四军医大学西京医院神经外科,陕西西安710032 [3]第四军医大学口腔医院药剂科,陕西西安710032
基金项目:国家自然科学基金资助项目(编号81200949);国家自然科学基金资助项目(编号30930093);十二五国家科技支撑计划课题分题(编号2012BAIllB02);陕西省科技计划项目(编号2012JQ4005);西京医院学科助推计划(编号XJZTl2T05).
摘    要:目的探讨藏红花素促进人脑胶质瘤细胞U87凋亡的作用及其机制。方法培养U87细胞系,随机分为二甲基亚砜对照组(对照组)和藏红花素治疗组(藏红花素组)。采用四甲基偶氮唑盐(MTT)法检测不同剂量藏红花素(低浓度组、中浓度组、高浓度组)对人胶质瘤细胞U87增殖的影响;流式细胞仪观察细胞凋亡情况。Western—blot检测ERK1/2,p-ERK1/2的表达变化。结果与对照组比较,藏红花素组U87细胞的生存率明显降低;随着藏红花素浓度增加,U87细胞的凋亡率显著上升(18.92%→51.68%→70.12%),组间差异有统计学意义(x2=14.102,P〈0.05);Western—blot结果显示,与对照组比较,藏红花素组的p-ERK1/2表达降低,而高浓度藏红花素组p-ERK1/2表达降低最显著,不同组间差异有统计学意义(P〈0.05)。结论藏红花素可能呈剂量依赖性的通过抑制。p-ERK1/2但讲TIR7缃晌桶广学垤雷尊的精肿瘤作用

关 键 词:藏红花素  U87胶质瘤细胞  凋亡  剂量依赖性  p—ERK1  2

Mechanism research of Crocin inducing apoptosis of human glioma cell strain U87
BIAN Huan,ZHANG Lei,WANG Rong,XIAO Xin,LI Juan,WANG Xiling,FEI Zhou.Mechanism research of Crocin inducing apoptosis of human glioma cell strain U87[J].China Medical Herald,2013(27):11-13.
Authors:BIAN Huan  ZHANG Lei  WANG Rong  XIAO Xin  LI Juan  WANG Xiling  FEI Zhou
Affiliation:1.Cadet Brigade Team 3, the Fourth Military Medical University in Shaanxi Province, Xi'an 710032, China; 2.De- partment of Neurosurgery, Xijing Hospital of the Fourth Military Medical University, Shaanxi Province, Xi' an 710032, China; 3.Department of Pharmacy, Stomatology Hospital of the Fourth Military Medical University, Shaanxi Province, Xi'an 710032, China)
Abstract:Objective To study the mechanism of Crocin inducing apoptosis of human glioma cell strain U87. Meth- ods The U87 cells were cultured and randomly divided into Dimethyl Sulphoxide group (control group) and Crocin treatment group (Crocin group). MTT assay was used to measure the influence of different concentrations of Crocin (L Crocin group, M Crocin group, H Crocin group) on proliferation of U87 cells. The apoptosis of U87 cells was detected by flowcytometry. The ERK1/2, p-ERK1/2 were detected by Western-blot. Results Compared with control group, via- bility of U87 cells in Crocin group was significantly reduced, with the increase of concentration of Crocin, U87 cell apoptosis rate increased significantly (18.92%→51.68%→70.12%, X2=14.102, P 〈 0.05); the Western-blot results showed that compared with control group, the p-ERK1/2 expression in U87 cells of Crocin group reduced, and p- ERK1/2 expression of H Croein group reduced most significant, p-ERK1/2 expression between L Crocin group, M Croein group, H Crocin group was significant (/9 〈 0.05). Conclusion Crocin may induce apoptosis of U87 cells by the inhibite of p-ERK1/2 with dose-dependent, and plays important anti-glioma role.
Keywords:Crocin  U87 glioma cells  Apoptosis  Dose-dependent  P-ERK1/2
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