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神经营养因子3抑制地塞米松诱导小鼠MC3T3-E1成骨细胞凋亡的作用及机制
作者单位:;1.西安交通大学第一附属医院风湿免疫科
摘    要:目的:研究神经营养因子3(NT-3)抑制地塞米松(DEX)诱导小鼠MC3T3-E1成骨细胞凋亡的作用及机制。方法:培养小鼠MC3T3-E1成骨细胞并分组,对照组用不含药物的DMEM处理,DEX组用含有5μmol/L地塞米松的DMEM处理、NT-3组用含有5μmol/L地塞米松及100 ng/mL NT-3的DMEM处理。检测细胞凋亡率、增殖活力、成骨标志物的含量、凋亡基因及PI3K/AKT/mTOR信号通路分子的表达量。结果:DEX组的细胞凋亡率及细胞中bax、caspase-3的表达量明显高于对照组,增殖活力值、培养基中ALP、OCN、COL-I的含量及细胞中bcl-2、p-PI3K、p-AKT、p-mTOR的表达量明显低于对照组(P<0.05);NT-3组的细胞凋亡率及细胞中bax、caspase-3的表达量明显低于DEX组,增殖活力值、培养基中ALP、OCN、COL-I的含量及细胞中bcl-2、p-PI3K、p-AKT、p-mTOR的表达量明显高于DEX组(P<0.05)。结论:NT-3对地塞米松诱导小鼠MC3T3-E1成骨细胞凋亡具有抑制作用且该作用可能的机制是激活PI3K/AKT/mTOR信号通路。

关 键 词:神经营养因子3  地塞米松  成骨细胞  凋亡  PI3K/AKT/mTOR信号通路

Effect and mechanism of neurotrophin 3 on inhibiting dexamethasone-induced mouse MC3T3-E1 osteoblast apoptosis
Affiliation:Department of Rheumatology and Immunology, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, China;Department of Rheumatology and Immunology, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, China;Department of Rheumatology and Immunology, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, China;Department of Rheumatology and Immunology, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, China;Department of Rheumatology and Immunology, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, China;Department of Rheumatology and Immunology, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, China;Department of Rheumatology and Immunology, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, China
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