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首页> 外文期刊>Cell biology international. >Post-conditioning exacerbates the MnSOD immune-reactivity after experimental cerebral global ischemia and reperfusion in the rat brain hippocampus
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Post-conditioning exacerbates the MnSOD immune-reactivity after experimental cerebral global ischemia and reperfusion in the rat brain hippocampus

机译:后调节可加剧大鼠脑海马中实验性脑整体缺血和再灌注后的MnSOD免疫反应性

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摘要

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.
机译:这项研究通过在大鼠海马CA1和齿状回中检测到的MnSOD免疫反应性,监测了先前缺血发作后施加的亚致死性缺血(后调节)的影响。实验性的10分钟短暂性脑缺血,然后再灌注2天,然后对大鼠进行第二次缺血(适应后4或6分钟)。 5 h,1和2天后评估MnSOD免疫反应性。通过计算机显微光密度图像分析获得的结果表明,缺血后处理4分钟引起的MnSOD免疫反应性高于6分钟。但是,当MnSOD的产生较低时,在条件较强的条件下(6分钟)后,CA1神经元的活力较高,以及CA1和齿状回中MnSOD之间的差异表明,另一种机制将CA1神经元的促细胞凋亡目的地转变为抗凋亡。

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