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.
journal_name
Neuroreportjournal_title
Neuroreportauthors
Love S,Barber R,Srinivasan A,Wilcock GKdoi
10.1097/00001756-200008030-00030subject
Has Abstractpub_date
2000-08-03 00:00:00pages
2495-9issue
11eissn
0959-4965issn
1473-558Xjournal_volume
11pub_type
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