Abstract
A serine protease activated protein C has been shown to be a powerful neuroprotectant in stressed neurons and in hypoxic brain endothelium. In a clinically relevant model of embolic stroke in rodents, we now show that administration of activated protein C alone or in combination with tissue plasminogen activator, or both, 4 hours after embolic stroke improves the functional outcome and reduces brain infarction within 7 days of stroke. In contrast, tissue plasminogen activator alone was not protective. Thus, activated protein C may be useful as a new stand-alone therapy for clinical stroke and to extend the time window of thrombolytic therapy.
Publication types
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Comparative Study
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Research Support, N.I.H., Extramural
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Behavior, Animal
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Brain Edema / pathology
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Brain Edema / prevention & control
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Brain Infarction / etiology
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Brain Infarction / prevention & control
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Disease Models, Animal
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Drug Interactions
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Enzyme Activation / drug effects
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Male
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Motor Activity / drug effects
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Neuroprotective Agents / therapeutic use
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Protein C / metabolism*
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Protein C / therapeutic use
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Psychomotor Performance / drug effects
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Rats
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Rats, Wistar
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Recovery of Function*
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Stroke / complications
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Stroke / drug therapy
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Stroke / metabolism
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Stroke / physiopathology*
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Time Factors
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Tissue Plasminogen Activator / therapeutic use
Substances
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Neuroprotective Agents
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Protein C
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Tissue Plasminogen Activator