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首页> 外文期刊>Life sciences >Development of cerebral infarction, apoptotic cell death and expression of X-chromosome-linked inhibitor of apoptosis protein following focal cerebral ischemia in rats
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Development of cerebral infarction, apoptotic cell death and expression of X-chromosome-linked inhibitor of apoptosis protein following focal cerebral ischemia in rats

机译：大鼠局灶性脑缺血后脑梗死的发展，凋亡的死亡以及X染色体连锁的凋亡抑制因子的表达

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The aim of this study was to investigate the role of apoptosis or necrosis in the development of delayed infarct, and the relationship between the level of XIAP gene, caspase-3 activation and ischemic cell death following transient focal cerebral ischemia. Adult male Sprague-Dawley rats underwent right middle cerebral artery occlusion (MCAo) for 50 min and reperfusion for 0.5, 4, 8, 24 h, 3, 7, 14 days. On TTC-stained coronal sections, delayed infarct was observed to develop in the whole MCA territory, especially in frontoparietal cortex after ischemia. Near total infarct was shown in striatum 24 h after MCAo, while delayed infarct was evident in the cortex. By day 3, the infarct had progressively expanded to the nearly whole area of the frontoparietal cortex. Flow cytometric analysis of Annexin-V (marks apoptosis) and PI (propidium iodide, marks necrosis) labeling cells showed that MCAo dominantly induced necrosis in ischernic core, striaturn. Apoptosis contributed to delayed infarct and cell death in the border zone, dorsolateral cortex and hippocampus. The time-course of caspase-3 activation was consistent with the changes of apoptosis and infarct following MCAo. Further RT-PCR experiments indicated that there was a biphasic regulation of XIAP in time- and region-dependent manner after ischemia. In the infarct core (striatum), following a transient and slight increase during 0.5 h to 4 h post-MCAo, expression of XIAP mRNA markedly decreased. On the other hand, a longer and larger upregulation of XIAP was observed at early time points in border zone (0.5 to 8 h, in dorsolateral cortex; 0.5 to 24 h in hippocampus), then the level of XIAP reduced. A negative correlation was observed between apoptosis and regulation of XIAP gene in these regions. Our findings suggest a possible association between expression of XIAP gene, apoptosis and delayed infarct following ischemia. (c) 2005 Elsevier Inc. All rights reserved.
机译：这项研究的目的是调查凋亡或坏死在延迟性梗死发展中的作用，以及XIAP基因水平，caspase-3激活与短暂性局灶性脑缺血后缺血细胞死亡之间的关系。成年雄性Sprague-Dawley大鼠接受右脑中动脉闭塞（MCAo）50分钟，再灌注0.5、4、8、24 h，3、7、14天。在TTC染色的冠状切片上，观察到整个MCA区域都发生了延迟性梗塞，尤其是缺血后的前额叶皮层。 MCAo后24 h，纹状体中显示出近乎完全的梗塞，而皮质中则明显出现了梗塞延迟。到第3天，梗塞已逐渐扩大到额顶额叶皮层的几乎整个区域。 Annexin-V（标记凋亡）和PI（碘化丙啶，标记坏死）标记细胞的流式细胞仪分析表明，MCAo在缺血性纹状体纹状体中占主导地位。细胞凋亡导致边界区，背外侧皮层和海马的梗塞和细胞死亡延迟。 caspase-3激活的时间过程与MCAo继发后凋亡和梗死的变化一致。进一步的RT-PCR实验表明，缺血后XIAP呈时间和区域依赖性双相调节。在梗塞核心（纹状体）中，在MCAo后0.5 h至4 h短暂且轻微的增加后，XIAP mRNA的表达显着下降。另一方面，在边界区域的早期时间点（背外侧皮层0.5至8小时;海马体0.5至24小时）观察到XIAP的上调时间更长且更大，然后XIAP的水平降低。在这些区域中，凋亡与XIAP基因的调节之间存在负相关。我们的发现表明，XIAP基因的表达，细胞凋亡与缺血后延迟性梗死之间可能存在关联。 （c）2005 Elsevier Inc.保留所有权利。

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