Differences of calcium binding proteins immunoreactivities in the young hippocampal CA1 region from the adult following transient ischemic damage
Differences of calcium binding proteins immunoreactivities in the young hippocampal CA1 region from the adult following transient ischemic damage
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DOI：
10.1016/j.jns.2012.12.026
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发表时间：
2013-03-15
影响因子：
4.4
通讯作者：
Cho, Jun Hwi
中科院分区：
文献类型：
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作者：
Lee, Young Joo;Yan, Bing Chun;Cho, Jun Hwi
据报道，年轻人对短暂性脑缺血的抵抗力比成年人强得多。在本研究中，我们研究了约90%的成年沙鼠海马CA 1区锥体细胞在缺血再灌注后4天死亡，然而，在年轻的海马，约56%的人在缺血再灌注后7天死亡。我们比较了免疫反应和钙结合蛋白（CBPs），如钙结合蛋白28 k（CB-D28 k），钙视网膜蛋白（CR）和小清蛋白（PV）的水平。青年假手术组CBPs的免疫反应性和蛋白质水平均高于成年假手术组。缺血再灌注4d后，成人CBPs的免疫反应性和蛋白质水平均明显下降，而青年CBPs的免疫反应性和蛋白质水平明显维持。缺血再灌注后7天，青年组较成年组明显降低，但仍高于成年组。总之，短暂性脑缺血后4天，缺血CA 1区CBPs的免疫反应性和水平没有降低。这一发现表明，更长时间的CBPs的维护可能有助于减少和更多的延迟神经元死亡/损伤的年轻人。(c)2013爱思唯尔有限公司版权所有。
It has been reported that the young were much more resistant to transient cerebral ischemia than in the adult. In the present study, we examined that about 90% of CA1 pyramidal cells in the adult gerbil hippocampus died at 4 days after ischemia-reperfusion; however, in the young hippocampus, about 56% of them died at 7 days after ischemia-reperfusion. We compared immunoreactivities and levels of calcium binding proteins (CBPs), such as calbindin 28k (CB-D28k), calretinin (CR) and parvalbumin (PV). The immunoreactivities and protein levels of all the CBPs in the young sham were higher than those in the adult sham. In the adult, the immunoreactivities and protein levels of all the CBPs were markedly decreased at 4 days after ischemia-reperfusion, however, in the young, they were apparently maintained. At 7 days after ischemia-reperfusion, they were decreased in the young, however, they were much higher than those in the adult. In brief, the immunoreactivities and levels of CBPs were not decreased in the ischemic CA1 region of the young 4 days after transient cerebral ischemia. This finding indicates that the longer maintenance of CBPs may contribute to a less and more delayed neuronal death/damage in the young. (c) 2013 Elsevier B.V. All rights reserved.