Pericyte protection by edaravone after tissue plasminogen activator treatment in rat cerebral ischemia.
Pericyte protection by edaravone after tissue plasminogen activator treatment in rat cerebral ischemia.
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组织纤溶酶原激活剂治疗大鼠脑缺血后，埃达沃内的周细胞保护。
DOI：
10.1002/jnr.23420
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发表时间：
2014-11
影响因子：
4.2
通讯作者：
Abe, Koji
中科院分区：
文献类型：
--
作者：
Deguchi, Kentaro;Liu, Ning;Liu, Wentao;Omote, Yoshio;Kono, Syoichiro;Yunoki, Taijun;Deguchi, Shoko;Yamashita, Toru;Ikeda, Yoshio;Abe, Koji
周细胞在收缩、介导炎症和调节脑血流中起着关键作用。在这项研究中，神经血管单位（NVU）周细胞的变化与外源性组织纤溶酶原激活剂（tPA）和自由基清除剂依达拉奉的影响有关。免疫组织化学和Western blot分析显示，在短暂性大脑中动脉闭塞（tMCAO） 90分钟后4天，血小板源性生长因子受体β阳性周细胞和n -乙酰氨基葡萄糖寡聚物（NAGO）阳性内皮细胞之间的重叠明显增加。周细胞数量和与NAGO的重叠随着tPA的增加而减少，但在tMCAO后4天依达拉奉恢复并增殖。因此，tPA治疗损伤周细胞，导致星形胶质细胞脱离，胶质细胞系来源的神经营养因子分泌减少。然而，依达拉奉治疗大大改善了tpa诱导的周细胞损伤。本研究表明外源性tPA强烈损伤周细胞，破坏NVU的完整性，但依达拉奉治疗可显著改善大鼠急性脑缺血后的这种损伤。©2014作者。Wiley期刊公司出版的神经科学研究杂志。
Pericytes play a pivotal role in contraction, mediating inflammation and regulation of blood flow in the brain. In this study, changes of pericytes in the neurovascular unit (NVU) were examined in relation to the effects of exogenous tissue plasminogen activator (tPA) and a free radical scavenger, edaravone. Immunohistochemistry and Western blot analyses showed that the overlap between platelet-derived growth factor receptor β-positive pericytes and N-acetylglucosamine oligomers (NAGO)-positive endothelial cells increased significantly at 4 days after 90 min of transient middle cerebral artery occlusion (tMCAO). The number of pericytes and the overlap with NAGO decreased with tPA but recovered with edaravone 4 days after tMCAO with proliferation. Thus, tPA treatment damaged pericytes, resulting in the detachment from astrocytes and a decrease in glial cell line-derived neurotrophic factor secretion. However, treatment with edaravone greatly improved tPA-induced damage to pericytes. The present study demonstrates that exogenous tPA strongly damages pericytes and destroys the integrity of the NVU, but edaravone treatment can greatly ameliorate such damage after acute cerebral ischemia in rats. © 2014 The Authors. Journal of Neuroscience Research Published by Wiley Periodicals, Inc.
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2.1
作者：
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