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Involvement of Apoptosis in 3-nitropropionic Acid-induced Ischemicl Tolerance to Transient Focal Cerebral Ischemia in Rats
引用本文:朱红灿,孙圣刚,李红戈,童萼塘. Involvement of Apoptosis in 3-nitropropionic Acid-induced Ischemicl Tolerance to Transient Focal Cerebral Ischemia in Rats[J]. 华中科技大学学报(医学英德文版), 2004, 24(1): 79-82. DOI: 10.1007/BF02830713
作者姓名:朱红灿  孙圣刚  李红戈  童萼塘
作者单位:Department of Neurology,Department of Neurology,Department of Neurology,Department of Neurology Union Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430022,Union Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430022,Union Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430022,Union Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430022
基金项目:ThisprojectwassupportedbyagrantfrominitiativeFoundationofNatioualEducationMinistryforscholarscomingbackfromothercountries (No .2 0 0 1 345)
摘    要:Preconditioningofbraintissueswithsub lethalstressesorstimulicanresultinresistancetosubse quentlethalischemiceventsinaresponsecalledis chemictolerance .Recently ,severalstudieshaveshownthatasinglesystemicdoseof 2 0mg/kg 3 NPAcausednohistopathologicalabnorm…

关 键 词:短暂性脑缺血 缺血耐受 细胞凋亡 3-硝基丙酸 动物实验
收稿时间:2003-06-02

Involvement of apoptosis in 3-nitropropionic acid-induced ischemic tolerance to transient focal cerebral ischemia in rats
Zhu Hongcan,Sun Shenggang,Li Hongge,Tang Etong. Involvement of apoptosis in 3-nitropropionic acid-induced ischemic tolerance to transient focal cerebral ischemia in rats[J]. Journal of Huazhong University of Science and Technology. Medical sciences, 2004, 24(1): 79-82. DOI: 10.1007/BF02830713
Authors:Zhu Hongcan  Sun Shenggang  Li Hongge  Tang Etong
Affiliation:Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology,Wuhan 430022
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.
Keywords:3-nitropropionic acid  cerebral ischemic tolerance  ischemic penumbra  apoptosis
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