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Leptomycin B ameliorates vasogenic edema formation induced by status epilepticus via inhibiting p38 MAPK/VEGF pathway

Authors
Kim, Duk-SooMin, Su-JiKim, Min-JuKim, Ji-EunKang, Tae-Cheon
Issue Date
15-Nov-2016
Publisher
Elsevier BV
Keywords
Epilepsy; Seizure; Leptomycin B; P38 MAPK; VEGF; Piriform cortex
Citation
Brain Research, v.1651, pp 27 - 35
Pages
9
Journal Title
Brain Research
Volume
1651
Start Page
27
End Page
35
URI
https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/8600
DOI
10.1016/j.brainres.2016.09.023
ISSN
0006-8993
1872-6240
Abstract
The blood-brain barrier (BBB) disruption during brain insults leads to vasogenic edema as one of the primary steps in the epileptogenic process. However, the signaling pathway concerning vasogenic edema formation has not been clarified. In the present study, status epilepticus (SE) resulted in vascular endothelial growth factor (VEGF) over-expression accompanied by loss of BBB integrity in the rat piriform cortex. Leptomycin B (LMB, an inhibitor of chromosome region maintenance 1) attenuated SE-induced vasogenic edema formation. This anti-edema effect of LMB was relevant to inhibitions of VEGF over expression as well as p38 mitogen-activated protein kinase (MAPK) phosphorylation. Furthermore, 513202190 (a p38 MAPK inhibitor) ameliorated vasogenic edema and VEGF over-expression induced by SE. These findings indicate that p38 MAPK/VEGF signaling pathway may be involved in BBB disruption following SE. Thus, we suggest that p38 MAPK/VEGF axis may be one of therapeutic targets for vasogenic edema in various neurological diseases. (C) 2016 Elsevier B.V. All rights reserved.
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