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Involvement of oxidative stress and caspase-3 in cortical infarction after photothrombotic ischemia in mice.

Authors
 Gyung W. Kim  ;  Taku Sugawara  ;  Pak H. Chan 
Citation
 Journal of Cerebral Blood Flow and Metabolism, Vol.20(12) : 1690-1701, 2000 
Journal Title
 Journal of Cerebral Blood Flow and Metabolism 
ISSN
 0271-678X 
Issue Date
2000
MeSH
Animals ; Antibodies ; Antioxidants/pharmacology ; Blood-Brain Barrier/physiology ; Blotting, Western ; Brain Ischemia/drug therapy ; Brain Ischemia/metabolism* ; Caspase 3 ; Caspases/analysis ; Caspases/immunology ; Caspases/metabolism* ; Cerebral Cortex/blood supply ; Cerebral Cortex/metabolism ; Cerebral Infarction/drug therapy ; Cerebral Infarction/metabolism* ; Cerebrovascular Circulation/drug effects ; Cerebrovascular Circulation/physiology ; Cytochrome c Group/metabolism ; Cytosol/enzymology ; DNA Fragmentation ; Free Radical Scavengers/pharmacology ; In Situ Nick-End Labeling ; Intracranial Thrombosis/drug therapy ; Intracranial Thrombosis/metabolism* ; Male ; Mice ; Mice, Inbred Strains ; Oxidative Stress/drug effects ; Oxidative Stress/physiology* ; Pregnatrienes/pharmacology
Keywords
Oxidative stress ; Photothrombotic ischemia ; Caspase-3 ; DNA fragmentation
Abstract
Apoptosis-related cell death is linked to oxidative stress and caspases in experimental cerebral ischemia, However, the role of oxidative stress in caspase activation and subsequent apoptotic cell death after cerebral ischemia is unknown, The authors evaluated the role of oxidative stress in ischemic cerebral infarction after photothrombosis and the relation between oxidative stress and caspase-related cell death 6 and 24 hours after ischemia with and without U-74389G, a potent free radical scavenger (10 mg/kg, 30 minutes before and after ischemia induction). Reactive oxygen species, detected by hydroethidine oxidation, and cytosolic cytochrome c were detected in early ischemic lesions. Western blot analysis showed the cleaved form and the level of the proform of caspase-3 in the ischemic lesion 24 hours after ischemia. Decreased caspase-3 immunoreactivity was detected in the antioxidant-treated group after ischemia. Decreased DNA fragmentation and laddering were detected and the lesion was smaller in the treated group after ischemia compared with the untreated group. Oxidative stress and cytochrome c release occur in the ischemic lesion after photothrombotic ischemia. The free radical scavenger attenuated caspase-3 up-regulation, DNA fragmentation, and the final lesion. The authors concluded that oxidative stress may mediate caspase-related apoptotic cell death and subsequent cortical infarction after photothrombotic ischemia.
Full Text
http://journals.sagepub.com/doi/abs/10.1097/00004647-200012000-00008
DOI
10.1097/00004647-200012000-00008
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Neurology (신경과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Gyung Whan(김경환) ORCID logo https://orcid.org/0000-0001-7053-4372
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/171684
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