核因子-κB在急性脑缺血再灌注损伤中的作用及地塞米松的影响

CEREBRAL ISCHEMIA-REPERFUSION STIMULATED NF-κB ACTIVATION AND THE EFFECT OF DEXAMETHASONE IN MICE

目的 :观察小鼠急性脑缺血再灌注损伤时核因子 -κB(nuclearfactor-kappaB ,NF -κB)活性变化及作用和地塞米松 (dexamethasone,DXM )的影响。方法 :小鼠随机分为 :假手术组 ;脑缺血组 ;缺血再灌注 2h组 ;DXM预处理组 ;制备小鼠急性脑缺血再灌注模型并于缺血 2 0min和再灌注 2h后断头取脑 ;同时记录异常神经症状 ;用免疫组织化学法检测脑组织中NF -κB亚单位P6 5活性。结果 :脑缺血再灌注 2hP6 5活性增加 (P<0 .0 5 ) ,DXM预处理能降低P6 5活性水平 (P <0 .0 5 ) ;且能明显改善小鼠脑缺血再灌注损伤后的异常神经症状 (P <0 .0 5 )。结论 :NF -κB参与了小鼠急性脑缺血再灌注早期损伤的过程 ;地塞米松可能通过抑制NF-κB活性减轻缺血再灌注早期损伤。

Objective:To observe the activation of nuclear factor-kappa B(NF-κB)and the effect of dexamethasone (DXM) on NF-κB activityof mice with cerebral is chemia andreperfusion .Methods:The cerebral ischemia and reperfusion model in mice was made bymeans of ligatmg bilateral common carotid arteries and bleeding for 0.3ml in tail; adult mousewere randomly divided into four groups: sham operation group,cerebral ischemical group, expertmental group with cerebral ischemia- reperfusion for 2h and DXM pretreatment group. Immunohistochemical were used to evaluate NF-κB subunit P65 activity in cerebral cortex Meanwhile, abnormal nervous symptoms was recorded.Results:Significantly increased activity of P65 in expertmental group( P <0.05), After DXM pretreatment P65 activity became lower( P <0.05), and abnormal nervous symptoms was also improved( P <0.05) .Conclusions:It is suggest that dexamethasone have some protective effects against cerebral ischemia and reperfusion injury at early stage and that protection seemed to be related to inhibiting augmentation of NF-κB activity.