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.
Artigo
em Inglês
| WPRIM
| ID: wpr-330866
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.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Patologia
/
Propionatos
/
Dano ao DNA
/
Traumatismo por Reperfusão
/
Córtex Cerebral
/
Ataque Isquêmico Transitório
/
Circulação Cerebrovascular
/
Apoptose
/
Precondicionamento Isquêmico
/
Artéria Cerebral Média
Limite:
Animais
Idioma:
Inglês
Revista:
Journal of Huazhong University of Science and Technology (Medical Sciences)
Ano de publicação:
2004
Tipo de documento:
Artigo
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