Transgenic over-expression of slit2 enhances disruption of blood-brain barrier and increases cell death after traumatic brain injury in mice
Transgenic over-expression of slit2 enhances disruption of blood-brain barrier and increases cell death after traumatic brain injury in mice
复制标题
转基因过度表达slit2可增强小鼠脑外伤后血脑屏障的破坏并增加细胞死亡
DOI：
10.1016/j.neulet.2016.08.013
复制
发表时间：
2016-09-19
影响因子：
2.5
通讯作者：
Zhang, Yu
中科院分区：
文献类型：
--
作者：
Li, Shuai;Li, Hang;Zhang, Yu
创伤性脑损伤（TBI）是男性青少年和年轻人死亡和残疾的主要原因;轻度创伤性脑损伤是最常见的创伤性脑损伤类型。血脑屏障（blood-brain barrier，BBB）的破坏在脑外伤中起重要作用。以前，我们已经发现，slit 2，狭缝蛋白家族的成员，增加血脑屏障的通透性。在本研究中，我们研究了slit 2在小鼠微小TBI模型中轻度TBI发病机制中的作用。罗丹明BandP 1（Propidiumlodide）染色分别检测血脑屏障通透性和细胞死亡。与C57对照组小鼠相比，Slit 2-Tg小鼠微量TBI后罗丹明B的渗漏和细胞死亡显著增加。目前的结果表明，slit 2的过度表达在轻度TBI的病理生理学中起着有害的作用。(C)2016作者（S）由Elsevier爱尔兰有限公司发布。这是CC BY-NC-ND许可证下的开放获取文章（http：//creativecommons.org/licenses/by-nc-nd/4.0/）。
Traumatic brain injury (TBI) is the leading cause of mortality and disability among male adolescents and young adults; and mild traumatic brain injury is the most common type of traumatic brain injury. The disruption of blood-brain barrier (BBB) plays an important role in brain trauma. Previously, we have found that slit2, a member of slit protein family, increases permeability of BBB. In the present study, we examined the role of slit2 in the pathogenesis of mild TBI in a mouse model of micro TBI. Rhodamine BandPl (Propidiumlodide) staining were used to detect the permeability of BBB and cell death, respectively. The leakage of Rhodamine B and cell death were significantly increased in Slit2-Tg mice than in C57 control mice after micro TBI. The present results suggest that over expression of slit2 plays a detrimental role in the pathophysiology of mild TBI. (C) 2016 The Author(s). Published by Elsevier Ireland Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).