Involvement of apoptosis in 3-nitropropionic acid-induced ischemic tolerance to transient focal cerebral ischemia in rats.
- Author:
Hongcan ZHU
1
;
Shenggang SUN
;
Hongge LI
;
E'tong TANG
Author Information
1. Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022.
- Publication Type:Journal Article
- MeSH:
Animals;
Apoptosis;
drug effects;
Cerebral Cortex;
blood supply;
Cerebrovascular Circulation;
DNA Damage;
Infarction, Middle Cerebral Artery;
pathology;
Ischemic Attack, Transient;
chemically induced;
pathology;
Ischemic Preconditioning;
Male;
Middle Cerebral Artery;
pathology;
Nitro Compounds;
Propionates;
Rats;
Reperfusion Injury;
pathology
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2004;24(1):79-82
- CountryChina
- Language:English
-
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.
