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癫痫持续状态后大鼠梨状皮层血管源性水肿形成前内皮素-1 表达上调。

Up-regulation of endothelial endothelin-1 expression prior to vasogenic edema formation in the rat piriform cortex following status epilepticus.

机构信息

Department of Emergency Medical Services, Eulji University, Seongnam, Gyeonggi-do 461-713, South Korea.

出版信息

Neurosci Lett. 2011 Aug 21;501(1):25-30. doi: 10.1016/j.neulet.2011.06.032. Epub 2011 Jun 29.

Abstract

Endothelin-1 (ET-1) is one of potential factors to induce vasogenic edema formation, since exogenous ET-1 treatment decreases aquaporin 4 (AQP4) expression and increases chemokines induction. To identify the role of endogenous ET-1 in vasogenic edema formation, we examined the correlation between endogenous ET-1 expression and vasogenic edema formation in the pirifom cortex following status epilepticus (SE). In the present study, SMI-71 (a brain-blood barrier marker) immunoreactivity was significantly reduced in blood vessels at 1 day after SE when vasogenic edema and neuronal damage were observed. ET-1 expression was up-regulated in endothelial cells prior to reduction in SMI-71 immunoreactivity. Furthermore, ET-1 expressing endothelial cells showed the absence of SMI-71 immunoreactivity. Increase in ET-1 expression was followed by reduced AQP4 immunoreactivity prior to vasogenic edema formation. Only a few microglia showed monocyte chemotactic protein-1 (a chemokine induced by ET-1) outside vasogenic edema lesion. Taken together, our findings suggest that endothelial ET-1 expression may contribute to SE-induced vasogenic edema formation via brain-blood barrier disruption at AQP4/MCP-1 independent manners.

摘要

内皮素-1(ET-1)是诱导血管源性水肿形成的潜在因素之一,因为外源性 ET-1 治疗会降低水通道蛋白 4(AQP4)的表达并增加趋化因子的诱导。为了确定内源性 ET-1 在血管源性水肿形成中的作用,我们研究了癫痫持续状态(SE)后梨状皮层中内源性 ET-1 表达与血管源性水肿形成之间的相关性。在本研究中,当观察到血管源性水肿和神经元损伤时,SE 后 1 天 SMI-71(血脑屏障标志物)免疫反应性在血管中显著降低。内皮细胞中的 ET-1 表达在 SMI-71 免疫反应性降低之前上调。此外,表达 ET-1 的内皮细胞显示缺乏 SMI-71 免疫反应性。在血管源性水肿形成之前,ET-1 表达增加会导致 AQP4 免疫反应性降低。只有少数小胶质细胞在血管源性水肿病变外显示单核细胞趋化蛋白-1(ET-1 诱导的趋化因子)。总之,我们的发现表明,内皮 ET-1 表达可能通过与 AQP4/MCP-1 无关的方式导致 SE 诱导的血管源性水肿形成。

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