摘要
①目的 研究脑缺血再灌注后大脑皮质及纹状体核转录因子 κB(NF κB)基因表达的变化规律及其与神经细胞凋亡的关系。②方法 应用线栓法建立大鼠大脑中动脉缺血 (MCAO)再灌注模型 ,原位杂交方法检测脑缺血 (1.5h)再灌注损伤不同时间点 (2、6、12h和 1、2、3、7、14d)皮质和纹状体NF κBp6 5mRNA表达及凋亡细胞的时程变化。③结果 脑缺血再灌注后 ,皮质NF κBp6 5mRNA的表达于缺血再灌注后 2h～ 3d明显升高 (t=6 .76～ 2 5 .0 6 ,P <0 .0 1) ;7～ 14d降至假手术组水平 (t =0 .5 1～ 1.31,P >0 .0 5 )。纹状体NF κBp6 5mRNA表达2h 开始升高 (t=5 .5 4 ,P <0 .0 5 ) ,6h～ 3d升高更为明显 (t=5 .6 6～ 4 4 .75 ,P <0 .0 1) ,7～ 14d恢复至假手术组水平 (t =1.15～ 1.19,P >0 .0 5 )。大脑皮质细胞凋亡数量于脑缺血 1.5h再灌注 2h～ 3d显著增加 (t =8.78～18.2 1,P <0 .0 1) ,2d达高峰 (t=18.2 1,P <0 .0 1) ,7～ 14d降至假手术组水平 (t=0 .18～ 2 .6 2 ,P >0 .0 5 ) ;纹状体细胞凋亡数于再灌注后 6h～ 3d升高明显 (t=9.12～ 2 6 .86 ,P <0 .0 1) ,7～ 14d恢复至假手术组水平 (t=0 .91～1.2 4 ,P >0 .0 5 )。细胞凋亡的时程变化与NF κBp6 5mRNA的表达基本一致。
ObjectiveTo observe the NF-κB expression in focal cerebral ischemia and reperfusion(FCIR), and to explore the effects of NF-κB on cell apoptosis.MethodsA FCIR model was made by thread embolism in middle cerebral artery. In situ hybridization was applied to observe the expression of NF-κB mRNA and to determine cell apoptosis at different time (2, 6, and 12 hours and 1, 2, 3, 7, and 14 days) after reperfusion of focal cerebral ischemia for 1.5 hours.ResultsIn the cortex, NF-κB p65 mRNA-positive neurons were observed 2 hours to 3 days after the reperfusion(t=6.76-25.06,P<0.01), and decreased to normal 7 days later(t=0.51-1.31,P>0.05). In the striatum, NF-κB p65 mRNA-positive neurons were observed 2 hours after reperfusion(t=5.54, P<0.05), expressed more evidently from 6 hours to 3 days(t=5.66-44.75,P<0.01), and decreased to normal 7 days later(t=1.15-1.19,P>0.05). The number of apoptotic cells in the cortex became more than normal 2 hours to 3 days after reperfusion (t=8.78-18.21,P<0.01),peaked at 2 d(t=18.21,P<0.01),and decreased to normal 7-14 days later( t=0.18-2.62,P>0.05). The apoptotic cells in the striatum were more than normal, in number, six hours to three days after reperfusion(t=9.12-26.86,P<0.01),and decreased to normal after 7 days(t=0.91-1.24,P>0.05).The change pattern of time-phase of apoptotic cells was similar to that of NF-κB in the cortex and striatum.ConclusionFCIR could increase the expression of NF-κB and induce cell apoptosis, and participate in the pathogenesis of cerebral ischemia and reperfusion injury. [
出处
《齐鲁医学杂志》
2004年第1期17-19,共3页
Medical Journal of Qilu
基金
山东省自然科学基金资助项目 (Y2 0 0 1C0 4
