低氧预处理对大鼠海马神经元缺氧耐受性和热休克蛋白表达的影响

被引:5
作者
丁爱石
王福庄
于顺
吴丽颖
赵彤
范明
机构
[1] 军事医学科学院基础医学研究所神经生物室!北京,军事医学科学院基础医学研究所神经生物室!北京,军事医学科学院基础医学研究所神经生物室!北京,军事医学科学院基础医学研究所神经生物室!北京,军事医学科学院基础医学研究所神经生物室!北京,军事
关键词
低缺预处理; 缺氧; 海马神经元; 细胞培养; Hsp70; 免疫组织化学;
D O I
暂无
中图分类号
R338.1 [神经原生理学];
学科分类号
0710 ; 071006 ;
摘要
采用免疫组织化学方法 ,观察低氧预处理对大鼠海马培养神经元缺氧耐受性和热休克蛋白(Hsp70 )表达的影响。结果显示 ,低氧预处理能诱导海马神经元对Hsp70的表达。经低氧预处理的海马神经元缺氧 复氧后Hsp70表达较对照组明显增强 ,神经元损伤程度减轻 ,神经元存活数明显高于对照组。本结果表明 ,低氧预处理可诱导海马培养神经元对Hsp70的表达 ,并使海马神经元对缺氧产生耐受 ,减少缺氧 复氧后神经元的死亡
引用
收藏
页码:51 / 54
页数:4
相关论文
共 9 条
[1]  
The heat shock stress response after brain lesions: induction of 72 kD heat shock protein(cell types involved, axonal transport, transcriptional regulation)and protein synthesis inhibition. Planas AM,Soriano MA,Estrada A,et al. Progress in Neurobiology . 1997
[2]  
Temporal profile of the effects of pretreatment with brief cerebral ischemia insult in the gerbil: cumulative damage and protective effects. Kato H,Liu Y,Arakik K,et al. Brain Research . 1991
[3]  
The proconditioned hippocampus accelerates Hsp 70 heat shock gene expression following transient ischemia in the gerbil. Aoki M,Abe K,Kawagoe J,et al. Neuroscience Letters . 1993
[4]  
Induced tolerance to ischemia in gerbil hippocampal neurons. Kirino T,Tsujta Y,Tamura A. Journal of Cerebral Blood Flow and Metabolism . 1991
[5]  
Neuron[P]. KUTKOVETSKYI VALENTYN YAKOVYCH;TURTI MARYNA VALENTYNIVNA.UA106289U,2016-04-25
[6]  
Induction of c-fos and heat shock protein after brief and prolonged cerebral ischemia in gerbils. Takemoto O,Tomimoto H,Yanagihara T. Stroke . 1995
[7]  
Effect of preceding in vivo sublethal ischemia on the evoked potentials during secondary in vitro hypoxia evaluated with gerbil hippocampal slices. Tokunaga H,Hiramatsu K,Sakaki T. Brain Research . 1998
[8]  
Protection of rat hippocampus against ischaemic neuronal damage by pretreatment with sublethal ischaemia. Liu Y,Kato H,nakata N,et al. Brain Research . 1994
[9]  
Effects of recombinant human Interleukin-6 on fos expression of cultured hippocampal neurons induced by anoxia. Ding AS,Wang FZ,Yang H,et al. Chin J Neuroimmunol Neurol . 1997