Involvement of apoptosis in 3-nitropropionic acid-induced ischemic tolerance to transient focal cerebral ischemia in rats / 华中科技大学学报(医学)(英德文版)
Journal of Huazhong University of Science and Technology (Medical Sciences)
; (6): 79-82, 2004.
Article
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| ID: wpr-330866
Biblioteca responsable:
WPRO
ABSTRACT
The involvement of apoptosis in mitochondrial toxin 3-nitropropionic acid (3-NPA)-induced ischemic tolerance to transient focal cerebral ischemia in rats and the mechanism was investigated. 3-NPA at a dose of 20 mg/kg or vehicle control was intraperitoneally into the rats. Three days later, rats were exposed to 2 h of middle cerebral artery occlusion followed by 24 h of reperfusion. Infarct volumes were assessed by 2,3,5-triphenyltetrazolinm chloride (TTC) staining 24 h after reperfusion. Neural cell apoptosis in cerebral ischemic penumbra was detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin in situ nick end labeling (TUNEL) and flow cytometry methods (FCM). The results showed that as compared to the vehicle-treated group, pretreatment with 3-NPA could reduce the infarct volume by 23.3% and decrease the number of TUNEL-positive neural cells and apoptotic percentage by 47% (P<0.05) and 44.9% (P<0.01), respectively. It was concluded that the development of 3-NPA-induced ischemic tolerance in brain might be related to the decreases in neural cell apoptosis.
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Asunto principal:
Patología
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Propionatos
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Daño del ADN
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Daño por Reperfusión
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Corteza Cerebral
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Ataque Isquémico Transitorio
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Circulación Cerebrovascular
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Apoptosis
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Precondicionamiento Isquémico
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Arteria Cerebral Media
Límite:
Animals
Idioma:
En
Revista:
Journal of Huazhong University of Science and Technology (Medical Sciences)
Año:
2004
Tipo del documento:
Article