摘要
目的 研究Wistar大鼠局灶脑缺血 /再灌注 (I/R)后脑组织中核因子 κB(NF κB)活化的基本规律及其意义。方法 线栓法闭塞大鼠右侧大脑中动脉 ,制备局灶I/R模型 ,分别于缺血 2h再灌注后 3、6、12、2 4h取脑组织做冰冻切片 ,用免疫组织化学法检测脑组织中NF κB核转位细胞。结果 正常大鼠脑组织中可见少许NF κB核转位细胞 ;R3h脑组织中NF κB核转位细胞较正常组有增加趋势 (P >0 .0 5 ) ,R6h增加明显 (P <0 .0 5 ) ,R12h增加达高峰 (P <0 .0 5 ) ,R2 4h明显回降并趋于正常水平 (P >0 .0 5 )。结论 I/R后脑组织中NF κB活化明显 ,R12h为活化高峰 ;I/R后脑组织中NF κB活化可能加剧了脑缺血损伤。
Objective To investigate the activation of nuclear factor kappa B and its significance in Wistar rat brain after focal cerebral ischemia/reperfusion.Methods A rat model of focal cerebral ischemia/reperfusion was made by filament occlusion of the right middle cerebral artery.At 3,6,12 and 24hours post-reperfusion,the cells with NF-κB nuclear translocation in rat brain were determined by immunohistochemistry.Results The level of NF-κB activation was relatively low,but the phenomenon of NF-κB nuclear translocation could be observed throughout brain in normal rats.There was an increase tendency in positive cells with NF-κB nuclear translocation at the R3h between I/Rsub-group and normal control group(P>0.05).And there was an obvious increase at the R6h (P<0.05),peaking at the R12h (P<0.05),and a sharp decrease at the R24h of I/R sub-group until approximately to the normal level(P>0.05).Conclusion Focal cerebral ischemia/reperfusion promotes the activation of NF-κB in the ischemic brain tissue which maybe play a neurodegeration role during cerebral ischemia/reperfusion injury.
出处
《重庆医学》
CAS
CSCD
2003年第11期1496-1498,共3页
Chongqing medicine
基金
国家自然科学基金资助项目 (30 0 4 0 0 1 3)
重庆市科委应用基础项目 (渝科计 [2 0 0 2 ] 1 8 93)
重庆市卫生局中医药科研计划项目 (渝中医 [2 0 0 2 ] 4 2 30 )
关键词
局灶脑缺血
再灌注
核因子-ΚB
核转位
免疫组织化学
大鼠
脑组织
focal cerebral ischemia/reperfusion
nuclear factor kappa B
nuclear translocation
immunohistochemistry
rat
