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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。
Objective: To investigate the protective effect and mechanism of stromal cell-derived factor 1α (SDF-1α) on human glioma U87 cells injured by hydrogen peroxide (H2O2). The effects of SDF-1α on the proliferation of U87 cells were investigated by cell proliferation assay. After 12 hours of U87 treatment, SDF-1α cells were treated with SDF- 0.7 mM H2O2 for 6 hours, and the apoptosis rate was detected by flow cytometry. The protein expression of Akt and ERK1 / 2) the impact of phosphorylation. Results: SDF-1α was almost not secreted by glioma U87 itself, and exogenous SDF-1α had no effect on the proliferation of U87 cells within 24 hours. After H2O2 injury, the survival rate of SDF-1α pretreatment group was higher than that of control group The mortality and mortality were lower than those in the control group, and the difference was statistically significant. Western blot showed that SDF-1α could induce the rapid phosphorylation of Akt and ERK1 / 2 in U87 cells. Conclusion: SDF-1α can increase the survival rate of U87 cells induced by H2O2 and reduce the apoptosis rate and mortality rate. The mechanism may be related to PI3K-Akt and mitogen-activated protein kinase (MAPK) -ERK1 / 2 pathway related to the activation.