rh-CSF1改善缺糖缺氧损伤神经元线粒体功能和细胞凋亡
The rh-CSF1 improves mitochondrial function and cell apoptosis in neurons under oxygen-glucose deprivation
刘蕊 1范宽 1张鹏举 1田雨 1司玮 1李世容 1王露 1顾然 1胡晓1
作者信息
- 1. 贵州省人民医院神经内科(贵阳 550000)
- 折叠
摘要
目的 探讨集落刺激因子-1(colony stimulating factor-1,CSF1)抑制氧糖剥夺(oxygen-glucose depriva-tion,OGD)神经元凋亡的作用机制.方法 采用大鼠原代大脑皮质神经元,分为OGD损伤神经元模型组(OGD组,n=3)、重组人CSF1(recombined human CSF1,rh-CSF1)干预组(rh-CSF1组,n=3)、对照组(n=3).测定3组神经元凋亡率和其中三磷酸腺苷(adenosine triphosphate,ATP)含量,活性氧簇水平、线粒体膜电位和线粒体脱氧核糖核酸(deoxyribonucleic acid,DNA)拷贝数,检测线粒体内丙二醛含量和超氧化物歧化酶活性.结果 OGD组模型进行基线评估,结果示神经元凋亡率、活性氧簇、线粒体内丙二醛水平、线粒体膜电位、线粒体DNA拷贝数、ATP含量、线粒体内超氧化物歧化酶活性与对照组有统计学差异(P<0.01).rh-CSF1干预可提高OGD损伤后神经元的线粒体膜电位(0.55±0.03 vs.0.43±0.06,P<0.01)、线粒体DNA拷贝数(0.88±0.05 vs.0.72±0.06,P<0.05)、ATP含量[(15.70±0.99)mmol/mg vs.(11.70±1.00)mmol/mg,P<0.01)]和线粒体内超氧化物歧化酶活性[(18.47±1.38)U/mg vs.14.78±1.81)U/mg,P<0.05)],降低活性氧簇(3.64±0.21 vs.4.45±0.33,P<0.05)和线粒体内丙二醛水平[(2.13±0.19)mmol/mg vs.(2.78±0.20)mmol/mg,P<0.05)],减轻神经元凋亡率.结论 rh-CSF1可能通过改善线粒体功能、减轻氧化应激及抑制细胞凋亡,从而改善OGD诱导损伤神经元的受损程度.
Abstract
Objective To investigate the mechanism by which Colony Stimulating Factor-1(CSF1)inhibits apoptosis in neurons subjected to oxygen-glucose deprivation(OGD).Methods Primary rat cortical neurons were divided into the OGD damaged neuron model group(OGD group),the rh-CSF1 intervention group(rh-CSF1 group),and control group.The sample size for each group was 3.After intervention with recombinant human CSF1(rh-CSF1),neuronal apoptosis rate and intracellular ATP content,reactive oxygen species levels,mitochondrial membrane potential,and mitochondrial DNA copy number were measured.The content of malondialdehyde within mitochondria and the activity of superoxide dismutase were also assessed.Results Intervention with rh-CSF1 increased mitochondrial membrane potential(0.55±0.03 vs.0.43±0.06,P<0.01),mitochondrial DNA copy number(0.88±0.05 vs.0.72±0.06,P<0.05),ATP content[(15.70±0.99)mmol/mg vs.(11.70±1.00)mmol/mg,P<0.01)],and superoxide dismutase[(18.47±1.38)U/mg vs.(14.78±1.81)U/mg,P<0.05)]activity in neurons injured by OGD.It also reduced levels of rectivereactive oxygen species(3.64±0.21 vs.4.45±0.33,P<0.05)and malondialdehyde within mitochondria[(2.13±0.19)mmol/mg vs.(2.78±0.20)mmol/mg,P<0.05)],and inhibited neuronal apoptosis(10.12±0.78 vs.17.04±1.23,P<0.01)Conclusion rh-CSF1 may alleviate the damage in neurons induced by OGD by improving mitochondrial function,reducing oxidative stress,and inhibiting cell apoptosis.
关键词
集落刺激因子-1/缺糖缺氧/凋亡/氧化应激/线粒体功能/缺血性脑卒中Key words
Colony stimulating factor-1/Oxygen-glucose deprivation/Apoptosis/Oxidative stress/Mitochon-drial function/Ischemic stroke引用本文复制引用
基金项目
国家自然科学地区科学基金项目(82060228)
贵州省高层次人才创新创业择优资助项目(2021)(05)
贵州省科技厅支撑计划(黔科合支撑[2021]一般077)
贵州省中医药管理局中医药、民族医药科学技术研究课题(QZYY-2023-052)
贵州省卫生健康委科学技术基金项目(gzwkj2023-006)
贵州省高层次创新型人才项目(黔科合平台人才-GCC[2023]029)
贵州省科学技术厅基础研究计划(黔科合基础-ZK[2023]一般225)
贵州省人民医院青年基金项目(GZSYQN202117)
贵州省高层次创新型人才"千层次"人才项目(GZSYQCC[2023]007)
出版年
2024
NETL
NSTL
万方数据