中文摘要：

目的：研究西比灵对沙鼠脑缺血再灌注后核因子-κB、单核细胞趋化蛋白-1表达的影响。方法：52只健康蒙古沙鼠随机分为正常对照组、假手术组、脑缺血再灌注（I/R）组、西比灵干预组,I/R组及西比灵干预组再分为6h、1d、3d、7d四个亚组。通过夹闭双侧颈总动脉10 min后松夹,建立沙鼠全脑缺血再灌注模型。采用免疫组化的实验方法检测各组脑组织中NF-κBp65、MCP-1的表达。结果：缺血再灌注后各时间点I/R组及西比灵干预组,NF-κBp65的表达量显著高于正常对照组及假手术组（均P〈0.01）,且出现MCP-1阳性表达。与I/R组比较,西比灵干预组在I/R后6h、1d,NF-κBp65、MCP-1表达下调（均P〈0.05）。结论：在脑缺血再灌注早期,西比灵能够下调NF-κBp65、MCP-1的表达,减轻局部炎症反应及脑缺血再灌注损伤。

英文摘要：

Objective： To investigate the effect of flunarizine on the expressions of NF-κB and MCP-1 in brain tissue following cerebral ischemia/reperfusion in gerbils. Methods： Fifty-tow healthy gerbils were randomly divided into four groups： normal control group, sham operated group, ischemia/reperfusion （UR）group and flunarizine intervention group. I/R group and flunarizine intervention group were subdivided into four reperfusion subgroups for 6h, 1d, 3d and 7d. The model of pan-cerebral ischemiaJreperfusion was established by blocking bilateral common carotid artery with non-injury artery clap for 10 minutes. The expressions of NF-κBp65 and MCP-1 were detected with immunohistochemistry method. Results： At 6h-7d post-I/R, the level of NF-κBp65 in I/R group and flunarizine intervention group was significantly higher than that of the normal control group and sham operated group （P〈0.01）, and the MCP-1 was explored. The expressions of NF-κB65 and MCP-1 were lower in flunarizine intervention group than in lfR group at the same time, which were in reperfusion for 6h and 1d respectively（P〈0.05）. Conclusions： During the early phase of cerebral ischemia/reperfusion, flunarizine can down-regulate the expressions of NF-κBp65 and MCP-1, and has neuroprotective effect against the local inflammatory reaction and ischemia/reperfusion injury.