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Text
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<a href="http://doi.org/10.1016/j.jns.2015.04.042" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.jns.2015.04.042</a>
Pages
37–45
Issue
1
Volume
354
Dublin Core
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Title
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Anti-edema action of thyroid hormone in MCAO model of ischemic brain stroke: Possible association with AQP4 modulation.
Publisher
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Journal of the neurological sciences
Date
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2015
2015-07
Subject
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Animals; Aquaporin 4/*physiology; Aquaporin-4; Brain Edema/*drug therapy/pathology; Cerebral edema; Cerebrovascular Circulation/drug effects/physiology; Diiodothyronines/*administration & dosage; Erythropoietin; Infarction; Injections; Intravenous; Ischemic brain stroke; Male; Mice; Middle cerebral artery occlusion (MCAO); Middle Cerebral Artery/*drug therapy/pathology; Stroke/*drug therapy/pathology; Thyroid hormone; Triiodothyronine/*administration & dosage
Creator
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Sadana Prabodh; Coughlin Lucy; Burke Jamie; Woods Robert; Mdzinarishvili Alexander
Description
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The use of neuroprotective strategies to mitigate the fatal consequences of ischemic brain stroke is a focus of robust research activity. We have previously demonstrated that thyroid hormone (T3; 3,3',5-triiodo-l-thyronine) possesses neuroprotective and anti-edema activity in pre-stroke treatment regimens when administered as a solution or as a nanoparticle formulation. In this study we have extended our evaluation of thyroid hormone use in animal models of brain stroke. We have used both transient middle cerebral artery occlusion (t-MCAO) and permanent (p-MCAO) models of ischemic brain stroke. A significant reduction of tissue infarction and a concurrent decrease in edema were observed in the t-MCAO model of brain stroke. However, no benefit of T3 was observed in p-MCAO stroke setting. Significant improvement of neurological outcomes was observed upon T3 treatment in t-MCAO mice. Further, we tested T2 (3,5-diiodo-l-thyronine) a natural deiodination metabolite of T3 in MCAO model of brain stroke. T2 potently decreased infarct size as well as edema formation. Additionally, we report here that T3 suppresses the expression of aquaporin-4 (AQP4) water channels which could be a likely mechanism of its anti-edema activity. Our studies provide evidence to stimulate clinical development of thyroid hormones for use in ischemic brain stroke.
Identifier
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<a href="http://doi.org/10.1016/j.jns.2015.04.042" target="_blank" rel="noreferrer noopener">10.1016/j.jns.2015.04.042</a>
Rights
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2015
Animals
Aquaporin 4/*physiology
Aquaporin-4
Brain Edema/*drug therapy/pathology
Burke Jamie
Cerebral edema
Cerebrovascular Circulation/drug effects/physiology
Coughlin Lucy
Department of Pharmaceutical Sciences
Department of Pharmacy Practice
Diiodothyronines/*administration & dosage
Erythropoietin
Infarction
Injections
Intravenous
Ischemic brain stroke
Journal of the neurological sciences
Male
Mdzinarishvili Alexander
Mice
Middle cerebral artery occlusion (MCAO)
Middle Cerebral Artery/*drug therapy/pathology
NEOMED College of Graduate Studies
NEOMED College of Pharmacy
Sadana Prabodh
Stroke/*drug therapy/pathology
Thyroid hormone
Triiodothyronine/*administration & dosage
Woods Robert