首都医科大学学报 ›› 2007, Vol. 28 ›› Issue (3): 337-340.

• 基础研究 • 上一篇    下一篇

氯化钴预处理对缺氧预适应小鼠海马组织HIF-1α表达的影响

邵国1, 高翠英1, 吕国蔚1,2   

  1. 1. 首都医科大学神经生物学系;2. 首都医科大学神经生物学系
  • 收稿日期:2006-09-05 修回日期:1900-01-01 出版日期:2007-06-24 发布日期:2007-06-24
  • 通讯作者: 吕国蔚

The Effects of CoCl2 Pretreatment on HIF-1α Expression in Hippocampus of Hypoxic Preconditioned Mice

Shao Guo1, Gao Cuiying1, Lü Guowei1,2   

  1. 1. Department of Neurobiology, Capital Medical University;2. Institute of Hypoxia Medicine, Capital Medical University
  • Received:2006-09-05 Revised:1900-01-01 Online:2007-06-24 Published:2007-06-24

摘要: 目的 检测氯化钴预处理后小鼠海马组织缺氧诱导因子-1α(HIF-1α)在急性重复氧过程中的变化及其可能的机制。方法 用数字表法将Balb/C小鼠随机分为氯化钴实验组和生理盐水对照组,2组动物分别在实验前3 h注射氯化钴和生理盐水,进行0次(H0)、1次(H1)、4次(H4)缺氧暴露,随即分别取海马组织,用Western blot及EMSA法检测HIF-1α蛋白质含量及HIF-1 DNA结合活性。结果 生理盐水预处理后,小鼠的缺氧耐受时间逐次显著递增;氯化钴预处理后缺氧耐受时间恒定增高。氯化钴预处理H0、H1、H4组海马组织的HIF-1α蛋白质含量差异未见统计学意义,但HIF-1 DNA结合活性在H1组升高、H4组降低。生理盐水预处理组海马组织的蛋白质含量及HIF-1 DNA结合活性在H0、H1、H4组均依次增加。结论 氯化钴预处理能显著增强小鼠对缺氧的耐受能力、激活海马组织中的HIF-1,但其分子机制可能与急性重复缺氧暴露增强缺氧耐受力的机制不同。

关键词: 氯化钴, 缺氧诱导因子-1, 海马, 小鼠

Abstract: Objective To investigate the effect of CoCl2 pretreatment on expression of HIF-1α in the hippocampus of hypoxic preconditioned mice.Methods Balb/c mice were randomly divided into group of CoCl2 and normal saline(NS),respectively injected with CoCl2 and NS 3 h before exposure to hypoxia for 0 run(H0),1 run(H1) and 4 runs(H4).The tissue of hippocampus was removed immediately after the exposure.Technique of Western blot and electrophoretic mobility shift assay(EMSA) were used to measure the HIF-1α protein level and HIF-1α DNA binding activity,respectively.Results The hypoxic tolerance time in group NS was significantly increased run by run but unchanged in group CoCl2.In group CoCl2,the level of HIF-1α protein was unchanged whereas HIF-1α DNA binding activity was increased in H1 and decreased in H4.In group NS,both HIF-1α protein and DNA binding activity were increased.Conclusion Hypoxic-tolerance of mice to hypoxia and HIF-1α in their hippocampus are,respectively,increased and activated by CoCl2 while its underlying molecular mechanisms are thought to be different from those induced by acute repetitive hypoxic exposure.

Key words: CoCl2, HIF-1α, hippocampus, mice

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