Abstract
Animal studies have shown brain ischaemia to cause oxidative damage to DNA and activation of caspase-3, leading to apoptosis. These changes may be exacerbated by reperfusion. To assess caspase-3 activation after transient and permanent brain ischaemia in man, we examined brain tissue from patients who had experienced a cardiac arrest with resuscitation or an atherothrombotic brain infarct, and died 12 h to 9 days later. Sections were immunostained for activated caspase-3 or the 89 kDa caspase-3-mediated cleavage product of poly(ADP-ribose) polymerase. Brain ischaemia caused activation of caspase-3 in macrophages/microglia. Some neurons showed delayed activation of caspase-3 after cardiac arrest, but very few in atherothrombotic infarcts. In man, activation of caspase-3 plays little part in neuronal death in atherothrombotic infarcts but may contribute to delayed death of neurons after cardiac arrest.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adult
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Aged
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Brain Ischemia / metabolism*
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Brain Ischemia / pathology
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Brain Ischemia / physiopathology
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Caspase 3
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Caspases / metabolism*
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Cell Death / physiology
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Cerebral Cortex / metabolism
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Cerebral Cortex / pathology
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Cerebral Cortex / physiopathology
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Cerebral Infarction / metabolism
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Cerebral Infarction / pathology
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Cerebral Infarction / physiopathology
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Child, Preschool
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Female
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Heart Arrest / complications
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Humans
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Intracranial Thrombosis / complications
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Intracranial Thrombosis / pathology
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Intracranial Thrombosis / physiopathology
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Macrophages / cytology
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Macrophages / metabolism
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Male
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Microglia / cytology
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Microglia / metabolism
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Middle Aged
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Nerve Degeneration / metabolism
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Nerve Degeneration / pathology
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Nerve Degeneration / physiopathology
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Neurons / metabolism
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Neurons / pathology
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Poly(ADP-ribose) Polymerases / metabolism
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Reperfusion Injury / metabolism*
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Reperfusion Injury / pathology
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Reperfusion Injury / physiopathology
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Resuscitation / adverse effects
Substances
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Poly(ADP-ribose) Polymerases
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CASP3 protein, human
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Caspase 3
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Caspases