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  

Effect and mechanism of neurotrophin 3 on inhibiting dexamethasone-induced mouse MC3T3-E1 osteoblast apoptosis

作　　者：樊萍[1] 冯秀媛[1] 胡楠 蒲丹[1] 吕晓虹[1] 孙怡宁[1] 何岚[1] FAN ping;FENG Xiu-yuan;HU Nan;PU Dan;LV Xiao-hong;SUN Yi-ning;HE Lan(Department of Rheumatology,The First Affiliated Hospital of Xi'an Jiaotong University,Xi'an 710061,China)

机构地区：[1]西安交通大学第一附属医院风湿免疫科

出　　处：《海南医学院学报》2019年第22期1698-1702,共5页Journal of Hainan Medical University

基　　金：国家自然科学基金(81900800);陕西省自然科学基础研究计划项目(2019JM-560)~~

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。Objective:To study the effect and mechanism of neurotrophin 3(NT-3)on inhibiting dexamethasone(DEX)-induced mouse MC3T3-E1 osteoblast apoptosis.Methods:Mouse MC3T3-E1 osteoblasts were cultured and divided into 3 groups.Control group were treated with DMEM without drugs;DEX group were treated with DMEM containing 5μmol/L dexamethasone,and NT-3 group were treated with DMEM containing 5μmol/L dexamethasone and 100ng/mL NT-3.Apoptosis rate,proliferation activity,osteogenesis marker contents as well as apoptosis gene and PI3K/AKT/mTOR signaling pathway molecule expression were detected.Results:The apoptosis rate as well as bax and caspase-3 expression in the cells of DEX group was significantly higher than those of control group,whereas proliferation activity value,ALP,OCN and COL-I contents in the medium as well as bcl-2,p-PI3K,p-AKT and p-mTOR expression in the cells were significantly lower than those of control group(P<0.05);the apoptosis rate as well as bax and caspase-3 expression in the cells of NT-3 group was significantly lower than those of DEX group,whereas proliferation activity value,ALP,OCN and COL-I contents in the medium as well as bcl-2,p-PI3K,p-AKT and p-mTOR expression in the cells were significantly higher than those of DEX group(P<0.05).Conclusion:NT-3 has inhibiting effect on the dexamethasone-induced mouse MC3T3-E1 osteoblast apoptosis,and the possible mechanism of this effect is to activate the PI3K/AKT/mTOR signaling pathway.

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 

分 类 号：R580[医药卫生—内分泌]