1.Involvement of apoptosis in 3-nitropropionic acid-induced ischemic tolerance to transient focal cerebral ischemia in rats.
Hongcan ZHU ; Shenggang SUN ; Hongge LI ; E'tong TANG
Journal of Huazhong University of Science and Technology (Medical Sciences) 2004;24(1):79-82
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.
Animals
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Apoptosis
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drug effects
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Cerebral Cortex
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blood supply
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Cerebrovascular Circulation
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DNA Damage
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Infarction, Middle Cerebral Artery
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pathology
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Ischemic Attack, Transient
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chemically induced
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pathology
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Ischemic Preconditioning
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Male
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Middle Cerebral Artery
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pathology
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Nitro Compounds
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Propionates
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Rats
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Reperfusion Injury
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pathology