Paravascular pathways contribute to vasculitis and neuroinflammation after subarachnoid hemorrhage independently of glymphatic control.
Paravascular pathways contribute to vasculitis and neuroinflammation after subarachnoid hemorrhage independently of glymphatic control.
复制标题
甲状腺蛛网膜下腔出血后独立于糖控制后，阵发途径会导致血管炎和神经炎症。
DOI：
10.1038/cddis.2016.63
复制
发表时间：
2016-03-31
影响因子：
9
通讯作者：
Su H
中科院分区：
文献类型：
--
作者：
Luo C;Yao X;Li J;He B;Liu Q;Ren H;Liang F;Li M;Lin H;Peng J;Yuan TF;Pei Z;Su H
蛛网膜下腔出血（Subarachnoid hemorrhage，SAH）是一种致死率极高的严重疾病。其病理并发症的机制尚未完全确定。在这里，我们调查的潜在参与胶质淋巴系统的神经病理学蛛网膜下腔出血。我们证明，SAH后血液成分迅速进入血管旁空间，并渗透到整个大脑的血管周围实质，造成灾难性的事件，如脑血管痉挛，迟发性脑缺血，微循环功能障碍和广泛的血管周围神经炎症。用组织型纤溶酶原激活剂清除血管旁通路可改善SAH的行为缺陷并减轻组织学损伤。有趣的是，与WT对照小鼠相比，AQP 4 −/−小鼠在SAH后第7天的神经功能缺损和神经炎症没有改善。总之，我们的研究证明，血管旁通路动态介导急性SAH后的病理并发症，独立于胶质淋巴控制。
Subarachnoid hemorrhage (SAH) is a devastating disease with high mortality. The mechanisms underlying its pathological complications have not been fully identified. Here, we investigate the potential involvement of the glymphatic system in the neuropathology of SAH. We demonstrate that blood components rapidly enter the paravascular space following SAH and penetrate into the perivascular parenchyma throughout the brain, causing disastrous events such as cerebral vasospasm, delayed cerebral ischemia, microcirculation dysfunction and widespread perivascular neuroinflammation. Clearance of the paravascular pathway with tissue-type plasminogen activator ameliorates the behavioral deficits and alleviates histological injury of SAH. Interestingly, AQP4−/− mice showed no improvements in neurological deficits and neuroinflammation at day 7 after SAH compared with WT control mice. In conclusion, our study proves that the paravascular pathway dynamically mediates the pathological complications following acute SAH independently of glymphatic control.