文章摘要
徐艳许余玲王军程洁肖杭△.SDF-1α对胶质瘤细胞U87 过氧化氢损伤的保护作用[J].,2011,11(12):2266-2268
SDF-1α对胶质瘤细胞U87 过氧化氢损伤的保护作用
Protective Effect of SDF-1α on Human Glioma Cell Line U87 Injuried byHydrogen Peroxide (H2O2) and Its Mechanism
  
DOI:
中文关键词: 基质细胞衍生因子1  U87  Akt  ERK1/2
英文关键词: Stromal cell derived factor-1  U87  Akt  ERK1/2
基金项目:江苏省普通高校研究生科研创新计划项目(CX09B_264Z);国家自然科学基金资助项目(编号:81072329)
作者单位
徐艳许余玲王军程洁肖杭△ 南京医科大学公共卫生学院神经毒理实验室 
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中文摘要:
      目的:探讨基质细胞衍生因子1α(SDF-1α)对过氧化氢(H2O2)损伤人脑胶质瘤细胞U87 的保护作用及机制。方法:双抗体夹 心酶联免疫吸附试验(ELISA) 检测胶质瘤细胞U87 自分泌SDF-1α;细胞增殖实验研究外源SDF-1α 对U87 细胞增殖的影响; SDF-1α 作用U87 12 小时后,0.7 mM H2O2 处理6 小时,流式细胞术检测细胞凋亡率;蛋白质免疫印记实验(western blot) 检测 SDF-1α 对U87 细胞中蛋白激酶B(Akt)和细胞外信号调节激酶1/2(ERK1/2)磷酸化的影响。结果:胶质瘤细胞U87 自身几乎不 分泌SDF-1α,24 小时内外源性SDF-1α 对U87 细胞增殖无明显影响;H2O2 损伤后,SDF-1α 预处理组细胞存活率高于对照组,凋 亡率和死亡率低于对照组,差异具有统计学意义;Western blot 显示SDF-1α 处理能够诱导U87 细胞Akt 和ERK1/2 的快速磷酸 化。结论:SDF-1α 能够提高H2O2 损伤的U87 细胞存活率,降低凋亡率和死亡率,其机制可能与磷脂酰肌醇3 激酶(PI3K)-Akt 和 丝裂原活化蛋白激酶(MAPK)-ERK1/2 通路的激活有关。
英文摘要:
      Objective: To investigate the protective effect and mechanism of stromal cell derived factor-1α (SDF-1α) on human glioma cell line U87 injuried by hydrogen peroxide (H2O2). Methods: Enzyme-linked Immunosorbent Assay was used to detect the SDF-1α produced by U87 cells. MTT Assay was performed to evaluate the effect of proliferation on cells induced by human recombinant SDF-1α. Then cells were divided into three groups: control group, H2O2 (0.7 mM) treated group, SDF-1α+H2O2 treated group (100 ng/ml and 0.7 mM respectively). Apoptotic cells were measured by flow cytometry. Western Blot was used to detect the expression of phosphorylated protein kinase B (pAkt) and phosphorylated extracellular signal regulating kinase (pERK1/2). Results: The human glioma cells treated by H2O2 exhibited apoptosis in the presence of SDF-1 compared with the cells treated with H2O2 alone. 100ng/ml SDF-1α treatement could lead to Akt and ERK activation in U87. Conclusion: SDF-1α could protect U87 cells from H2O2-induced apoptosis, the mechanism may be related to the activation of phosphatidylinositol 3-kinase (PI3K) -Akt and mitogen-activated protein kinase (MAPK) -ERK1/2 signalling pathway.
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