Abstract
In order to examine the effect of neurotrophin-3 (NT-3) on ischemic brain injury, NT-3 was topically applied to brain surface just after 90 min of middle cerebral artery occlusion (MCAO) in rats. NT-3 significantly reduced the infarct size at 24 h of reperfusion. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin in situ nick labeling (TUNEL) staining and immunohistochemical study for caspase-3 and heat shock protein 72 (HSP72) showed that NT-3 treatment decreased the number of cells with DNA fragmentation and caspase-3 and HSP72 expressions. These data suggest that NT-3 protects neuronal cells from ischemic injury, and it is possibly associated with inhibition of DNA fragmentation.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Administration, Topical
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Animals
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Apoptosis / drug effects
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Caspase 3
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Caspases / biosynthesis
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Cerebrovascular Circulation / drug effects
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DNA Fragmentation / drug effects
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Enzyme Induction / drug effects
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HSP72 Heat-Shock Proteins
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Heat-Shock Proteins / biosynthesis
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Immunohistochemistry
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In Situ Nick-End Labeling
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Infarction, Middle Cerebral Artery / drug therapy*
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Infarction, Middle Cerebral Artery / pathology
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Infarction, Middle Cerebral Artery / physiopathology
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Ischemic Attack, Transient / drug therapy*
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Ischemic Attack, Transient / pathology
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Ischemic Attack, Transient / physiopathology
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Middle Cerebral Artery / physiology*
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Neurotrophin 3 / administration & dosage
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Neurotrophin 3 / therapeutic use*
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Rats
Substances
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HSP72 Heat-Shock Proteins
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Heat-Shock Proteins
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Neurotrophin 3
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Casp3 protein, rat
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Caspase 3
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Caspases