摘要
目的 :探讨小剂量线粒体毒素 3 硝基丙酸 ( 3 nitoppropionicacid ,3 NPA)预处理对大鼠局灶性脑缺血脑梗死体积 ,脑缺血半暗带神经元凋亡的影响 ,阐明 3 NPA预处理诱导脑缺血耐受的机制。方法 :大鼠腹腔注射 3 NPA 3d后制作大脑中动脉闭塞模型 ,采用TTC染色、TUNEL法和流式细胞术 ,观察 3 NPA预处理对缺血 2h再灌注 2 4h脑梗死体积、神经元凋亡的影响。结果 :缺血 2h再灌注 2 4h ,3 NPA预处理组脑梗死体积变小 ,神经元凋亡减少 ,与对照组比有显著性差异。结论 :3 NPA预处理可以诱导脑缺血耐受 。
Aim:To investigate the involvement of apoptotic cells death in mitochondrial toxin 3-nitroprolpionic acid (3-NPA) induced ischemic tolerance to transient focal cerebral ischemia in rats.Methods:Rats were administrated either vehicle or 3-NPA at dose of 20 mg/kg,intraperitoneal,3 days prior to a 2 h middle cerebral artery occlusion followed by 24 h of reperfusion.Infarct volumes were assessed by a 2,3,5 triphenylte trazolinm chloride staining 24 h after reperfusion.The neural cells apoptosis in cerebral ischemic penumbra were measured by terminal deoxyncleotidyl transferase-mediated dUTP-tiotin in situ nick end labeling (TUNEL) and flow cytometry methods (FCM).Results:Treatment with 3-NPA exhibited a reduction in infarct volume.While,the neural cells apoptosis had a significant reduction as compared with the control group.Conclusion:The mechanism of the development of 3-NPA-induced ischemic tolerance in brain may relate to inhibit the apoptosis of neural cells.
出处
《中国临床神经科学》
2004年第1期20-22,共3页
Chinese Journal of Clinical Neurosciences
基金
教育部留学回国人员基金项目 (No .2 0 0 1 345)
关键词
3-硝基丙酸
预处理
局灶性脑缺血
神经元
凋亡
nitropropionic acid
cerebral ischemia
cerebral ischemic penumbra
apoptosis