| 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 |
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| 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） |
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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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