Ischemic Stroke Injury Is Reduced in Mice Lacking a Functional NADPH Oxidase
| Autor: | Joanne Mathias, G. Roger Thomas, Simon P. Green, John T. Curnutte, Walter C. Darbonne, Julie Rae, Claire E. Walder, Mary C. Dinauer |
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| Rok vydání: | 1997 |
| Předmět: |
Male
medicine.medical_specialty Pathology Ratón Neutrophile Ischemia Brain damage Brain Ischemia Pathogenesis Mice Superoxides Internal medicine medicine Animals Bone Marrow Transplantation Advanced and Specialized Nursing Oxidase test NADPH oxidase biology business.industry Cerebral infarction Brain NADPH Oxidases Cerebral Infarction medicine.disease Enzyme Activation Mice Inbred C57BL Endocrinology Mutation biology.protein Neurology (clinical) medicine.symptom Cardiology and Cardiovascular Medicine business |
| Zdroj: | Stroke. 28:2252-2258 |
| ISSN: | 1524-4628 0039-2499 |
| DOI: | 10.1161/01.str.28.11.2252 |
| Popis: | Background and Purpose Free radicals account for a significant proportion of the brain damage that occurs during ischemic stroke. Using mutant mice (X-CGD) with a dysfunctional phagocytic NADPH oxidase, we investigated the role of this superoxide-generating enzyme as a mediator of the reperfusion injury in a mouse model of middle cerebral artery occlusion. Methods Transient (2 hour) middle cerebral artery occlusion was performed in X-CGD or wild-type litter mates (8- to 10-week-old). After 22 hours of reperfusion, brains were harvested and infarct volume delineated using 2,3,5-triphenyltetrazolium chloride. To elucidate the origin of the damaging NADPH oxidase, transient ischemia was also performed in X-CGD or wild-type mice transplanted with wild-type C57 Bl/6J or X-CGD bone marrow, respectively. Results The infarct volume induced by transient ischemia was significantly less in X-CGD mice (29.1±5.6 mm 3 ; n=13) than wild-type littermates (54.0±10.6 mm 3 ; n=10; P Conclusions Brain injury was reduced in mice lacking a functional NADPH oxidase in both the central nervous system and peripheral leukocytes, suggesting a pivotal role for the NADPH oxidase in the pathogenesis of ischemia-reperfusion injury in the brain. |
| Databáze: | OpenAIRE |
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