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作 者:李卫华[1] 朱遂强[1] 唐荣华[1] 笱玉兰[1]
机构地区:[1]华中科技大学同济医学院附属同济医院神经内科,武汉430030
出 处:《神经损伤与功能重建》2006年第1期11-13,F0003,共4页Neural Injury and Functional Reconstruction
基 金:国家自然科学基金资助项目(30170333)
摘 要:目的:观测戊四氮(PTZ)及NF-κB圈套寡核苷酸结构对神经元样PC12细胞生长相关蛋白-43(GAP-43)表达的影响。方法:应用免疫印迹检测PTZ干预前后神经元样PC12细胞GAP-43的表达情况,进而运用基因转染技术将NF-κB圈套寡核苷酸转入神经元样PC12细胞中,应用激光共聚焦成像技术(CLSM)检测转染前后NF-κB的活性变化,免疫印迹观察转染前后GAP-43的变化情况。结果:①PTZ干预后神经元样PC12细胞GAP-43的表达显著增高;②CLSM检测显示转染NF-κB圈套寡核苷酸后神经元样PC12细胞中NF-κB活性明显下降,但GAP-43表达水平未降低。结论:PTZ可促进GAP-43的表达,NF-κB对GAP-43的表达不具有调控作用。Objective.. To investigate the effects of pentylenetetrazol (PTZ) and nuclear factor kappa B decoy oligodeoxynucleotides (NF-κB ODNs) on the expression of growth associated protein-43 (GAP-43)in neuron-like PC12 cell and to explore the epileptogenesis. Methods:The expression level of GAP-43 was studied by Western blot in neuron-like PC12 cells with and without PTZ treatment. NF-κB decoy ODNs were transfected into neuron-like PC12 ceils with Lipofectamine-2000, and confocal laser scanning microscope (CLSM) was performed to investigate the activation of NF-κB. Results: (1) Western blot showed that the level of GAP-43 was significantly increased in neuron-like PC12 cells with PTZ treatment when compared to the control cells. (2) CLSM showed that the decoy ONDs decreased the activation of NF-κB in neuron-like PC12 cell, while Western blot showed that the decoy ONDs did not decrease the level of GAP-43. Conclusion: PTZ can enhance the expression of GAP-43 and active NF-κB in PC12 cells. NF-κB could not modulate GAP 43 expression.
关 键 词:戊四氮 NF-κB圈套结构 GAP-43 神经元样细胞
分 类 号:R741[医药卫生—神经病学与精神病学] R742.1[医药卫生—临床医学]
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