摘要
目的研究银杏内酯抗脑缺血-再灌注损伤作用与线粒体ATP敏感性钾通道(mito K-ATP)开放的关系。方法用Longa法制作大鼠局灶性脑缺血-再灌注损伤模型。造模前静脉给予银杏内酯15 mg.kg-1和(或)选择性mito K-ATP拮抗剂5-羟基癸酸(5-HD)10 mg.kg-1预处理,以脑梗死体积、神经缺陷评分、SOD活性和丙二醛含量评价银杏叶提取物抗脑缺血-再灌注损伤的作用与mito K-ATP开放的关系。结果银杏内酯能够改善大鼠缺血-再灌注引起的脑功能和组织损伤,但此作用可被预先给予的5-HD减弱。结论银杏内酯抗脑缺血-再灌注损伤作用与mito K-ATP开放有关。
Objective To determine the relationship between the protection of bilobalide against focal cerebral ischemiareperfusion injury and mitochondrial ATP-sensitive potassium channels (mito K-ATP) in vivo. Methods A longa model was used in this study. Forty male Sprague-dawley rats were randomized into 4 groups (n= 10) : an model control group, a bilobalide group (15 mg·kg^-1), a 5 HD group (10 mg·kg^-1) and a 5-HD+bilobalide group. The neurological funciton was scored and the infarct volume, activity of SOD, and content of MDA were measured after the operation. Results In the 5-HD-kbilobalide group, the infarct volume and the neurological function were significantly higher than those in the bilobalide pretreated group. Conclusion The protective effect of bilobalide against focal cerebral ischemia-reperfusion injury may be related to mito K-ATP.
出处
《中南药学》
CAS
2009年第4期244-246,共3页
Central South Pharmacy
基金
湖南省医药卫生科研计划课题项目(编号:B2005116)
湖南省教育厅科研计划课题项目(编号:07C712)
关键词
银杏内酯
线粒体ATP敏感性钾通道
脑缺血-再灌注
bilobalide
mitochondrial ATP-sensitive potassium channels
cerebral ischemia-reperfusion