Post-conditioning exacerbates the MnSOD immune-reactivity after experimental cerebral global ischemia and reperfusion in the rat brain hippocampus
Post-conditioning exacerbates the MnSOD immune-reactivity after experimental cerebral global ischemia and reperfusion in the rat brain hippocampus
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DOI：
10.1016/j.cellbi.2007.08.023
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发表时间：
2008-01-01
影响因子：
3.9
通讯作者：
Burda, Jozef
中科院分区：
文献类型：
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作者：
Nemethova, Miroslava;Danielisova, Viera;Burda, Jozef
本研究监测的影响，亚致死性缺血（后处理）适用于以前的缺血发作后，通过MnSOD的免疫反应性检查在CA1和齿状回的大鼠海马。实验性短暂性脑缺血10 min后再灌注2 d，再进行第二次缺血（预处理后4或6 min）。MnSOD免疫反应性在5 h、1 d和2 d后进行评价。计算机显微光密度图像分析结果表明，4分钟的缺血后处理引起更高的MnSOD免疫反应性比6分钟。然而，较高的生存能力较强（6分钟）后处理时，生产的MnSOD较低，以及MnSOD在CA1和齿状回之间的差异表明另一种机制切换CA1神经元的促凋亡目的地的抗凋亡。(C)2007年国际细胞生物学联合会。由爱思唯尔有限公司出版。保留所有权利。
This study monitored the effects of sub-lethal ischemia (post-conditioning) applied after a previous ischemic attack by way of the MnSOD immune-reactivity examined in CA1 and dentate gyrus of the rat hippocampus. The experimental 10 min transient cerebral ischemia was followed by 2 days of reperfusion, the rats then underwent a second ischemia (4 or 6 min post-conditioning). MnSOD immune-reactivity was evaluated after 5 h, 1 and 2 days. Results obtained by computer microdensitometric image analysis indicated that 4 min of ischemic post-conditioning caused higher MnSOD immune-reactivity than 6 min. However, higher viability of CA1 neurons after stronger (6 min) post-conditioning when production of MnSOD is lower, as well as differences between MnSOD in CA1 and dentate gyrus indicates another mechanism switching pro-apoptotic destination of CA1 neurons to anti-apoptotic. (C) 2007 International Federation for Cell Biology. Published by Elsevier Ltd. All rights reserved.