Cell death starts early after subarachnoid hemorrhage.
Cell death starts early after subarachnoid hemorrhage.
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DOI：
10.1016/j.neulet.2012.01.036
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发表时间：
2012-03-14
影响因子：
2.5
通讯作者：
Sehba FA
中科院分区：
文献类型：
--
作者：
Friedrich V;Flores R;Sehba FA
脑损伤开始于动脉瘤性蛛网膜下腔出血（SAH）后的早期。虽然已知SAH后24小时脑内存在细胞凋亡和坏死，但尚不清楚SAH后细胞死亡开始的时间。我们之前已经描述了通过血管内穿刺诱导SAH后10分钟大鼠脑微血管的结构变化。这项研究在SAH诱导后10分钟检查了大脑细胞死亡的证据。在SAH后10分钟，血管和实质细胞中有明显的裂解caspase-3 （cl-caspase-3）染色，明显高于时间匹配的假手术对照组。SAH后24小时cl-caspase-3阳性细胞数量进一步增加。TUNEL检测显示，SAH后10分钟出现凋亡细胞，24小时出现更多凋亡细胞。SAH后1 h出现分散的Fluoro-Jade阳性神经元，并随时间增加。1小时时，皮层和皮层下有Fluoro-Jade阳性神经元，但海马中没有；24小时时，它们也出现在海马中，并且在血管穿刺的同侧半球中显著增加。假药未见氟玉染色。这些数据证明了SAH后内皮细胞和实质细胞凋亡和神经元坏死的早期激活，并确定了可以靶向减少SAH后早期脑损伤的终点。
Brain injury begins early after aneurysmal subarachnoid hemorrhage (SAH). Although cell death via apoptosis and necrosis is known to be present in brain 24 hours after SAH, it is not known how soon after SAH cell death begins. We have previously described structural changes in rat brain microvessels 10 minutes after induction of SAH by endovascular puncture. This study examined brain for evidence of cell death beginning 10 minutes after induction of SAH. Cleaved caspase-3 (cl-caspase-3) staining was evident in vascular and parenchymal cells at 10 minutes after SAH and was significantly greater than in time-matched, sham-operated controls. The number of cl-caspase-3 positive cells was increased further at 24 hour after SAH. TUNEL assay revealed apoptotic cells present at 10 minutes, with substantially more at 24 hours after SAH. Scattered Fluoro-Jade positive neurons appeared at 1 hour after SAH and their number increased with time. At 1 hour Fluoro-Jade positive neurons were present in cortical and subcortical regions but not in hippocampus; at 24 hours they were also present in hippocampus and were significantly greater in the hemisphere ipsilateral to the vascular puncture. No Fluoro-Jade staining was present in shams. These data demonstrate an early activation of endothelial and parenchymal cells apoptosis and neuronal necrosis after SAH and identifies endpoints that can be targeted to reduce early brain injury after SAH.
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