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The acquisition of ischemic tolerance in gerbil hippocampus.

沙鼠海马缺血耐受性的获得。

基本信息

批准号：
07680852
负责人：
SHIMAZAKI Kuniko
金额：
$ 1.41万
依托单位：
Jichi Medical School
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1995
资助国家：
日本
起止时间：
1995 至 1996
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-07680852/
关键词：
ischemia bcl-2 gerbil apoptosis CA1 tolerance to ischemia delayd neuronal death CA1 虚血神経細胞死海馬 bcl-2 スナネズミ

项目摘要

We previously reported that immunoreactivity of Bcl-2 greatly increased in the gerbil hippocampal CA1 sector in parallel with acquisition of tolerance for delayd neuronal death (Shimazaki et al., Neurosci.Res.1994).This finding suggests that bcl-2 may be an endogenous neuroprotectant. To confirm this hypothesis, we studied time course and location of bcl-2 protein and mRNA using gerbil model of sublethal brief ischemia. We have examined bcl-2 mRNA expression in the gerbil hippocampus by in situ hybridization and ribinuclease protection assay.The level of bcl-2 mRNA was markedly increased above 2 min of ischemicinsult. The bcl-2 mRNA was increased in CA1 and CA3 regions and the dentate gyrus (DG). Ribinuclease protection assay analysis supported the result showing marked increase in bcl-2 mRNA after both 2 min of ischemia and 5 min of ischemia. On the other hand no increase in the level of bcl-2 mRNA was found in the gerbil treated with 1 min ischemia. The results suggest close correlation between acquisition of tolerance for delayd neuronal death and expression of Bcl-2, which is known to support survival of the neuronal death. While bcl-2 mRNA was expressed in the hippocampal neurons after more than 2 min of ischemia. Bcl-2 protein was stlongly expressed in CA1 neurons that are rescured from cell death.

我们先前报道了Bcl-2的免疫反应性在沙鼠海马CA 1区大大增加，与获得延迟神经元死亡的耐受性平行（Shimazaki等，这一发现表明bcl-2可能是一种内源性神经保护剂。为了证实这一假设，我们研究了bcl-2蛋白和mRNA的时间过程和定位的沙土鼠亚致死短暂缺血模型。用原位杂交和核糖核酸酶保护实验检测了沙土鼠海马bcl-2 mRNA的表达，发现脑缺血2 min以上，bcl-2 mRNA的表达明显增加。bcl-2 mRNA在海马CA 1、CA 3区及齿状回（DG）表达增加。核糖核酸酶保护分析支持缺血2 min和5 min后bcl-2 mRNA均显著增加的结果。而缺血1 min组bcl-2 mRNA水平无明显升高。结果表明，延迟神经元死亡的耐受性的获得与Bcl-2的表达密切相关，Bcl-2已知支持神经元死亡的存活。缺血2 min以上海马神经元bcl-2 mRNA表达增加。Bcl-2蛋白在从细胞死亡中被拯救的CA 1神经元中持续表达。