Involvement of apoptosis in 3-nitropropionic acid-induced ischemic tolerance to transient focal cerebral ischemia in rats.
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.
Zhu
Hongcan
H
Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022.
Sun
Shenggang
S
Li
Hongge
H
Tang
E'tong
E
D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D002540:Cerebral Cortex / Q000098:blood supply; D002560:Cerebrovascular Circulation; D004249:DNA Damage; D020244:Infarction, Middle Cerebral Artery / Q000473:pathology; D002546:Ischemic Attack, Transient / Q000139:chemically induced / Q000473:pathology*; D019194:Ischemic Preconditioning; D008297:Male; D020768:Middle Cerebral Artery / Q000473:pathology; D009574:Nitro Compounds; D011422:Propionates; D051381:Rats; D015427:Reperfusion Injury / Q000473:pathology
D009574:Nitro Compounds; D011422:Propionates; C015392:3-nitropropionic acid