Journal
NEUROSCIENCE LETTERS
Volume 542, Issue -, Pages 92-96Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2013.02.051
Keywords
Hemorrhage; Stroke; Edema; Blood-brain barrier; Inflammation
Categories
Funding
- National Institute of Health [NS065172, NS075774]
- American Heart Association [BGIA2300135]
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Intracerebral hemorrhage (ICH), the most common form of hemorrhagic stroke, exhibits the highest acute mortality and the worst long-term prognosis of all stroke subtypes. Unfortunately, treatment options for ICH are lacking due in part to a lack of feasible therapeutic targets. Inflammatory activation is associated with neurological deficits in pre-clinical ICH models and with patient deterioration after clinical ICH. In the present study, we tested the hypothesis that R-7050, a novel cell permeable triazoloquinoxaline inhibitor of the tumor necrosis factor receptor (TNFR) complex, attenuates neurovascular injury after ICH in mice. Up to 2 h post-injury administration of R-7050 significantly reduced blood-brain barrier opening and attenuated edema development at 24 h post-ICH. Neurological outcomes were also improved over the first 3 days after injury. In contrast, R-7050 did not reduce hematoma volume, suggesting the beneficial effects of TNFR inhibition were downstream of clot formation/resolution. These data suggest a potential clinical utility for TNFR antagonists as an adjunct therapy to reduce neurological injury and improve patient outcomes after ICH. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
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