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作 者:邵恩得[1] 张静轩[1] 田世文[1] 张万兴[1] 王恒[1] 扈玉华[2]
机构地区:[1]河北省廊坊市人民医院神经外科,065000 [2]河北医科大学第二医院神经外科
出 处:《河北医药》2015年第13期1933-1935,共3页Hebei Medical Journal
摘 要:目的探讨胆囊收缩素-8(cholecystokinin-8,CCK-8)对实验性大鼠急性脑损伤后核因子-κB(necular factor kappa B,NF-κB)活性的影响。方法取成年Wistar大鼠60只,体重280~300 g,随机分为对照组、创伤组与CCK-8组。采用电泳迁移率改变分析方法(electrophoretic mobility shift assay,EMSA)检测核内NF-κB的活性,用免疫组化方法观察NF-κB在细胞内的表达情况,并用干湿重法测量损伤侧脑组织含水量。结果创伤组各时间点NF-κB的活性以及脑含水量较假手术组均有明显增高,而CCK-8组NF-κB的活性明显受到抑制,脑水肿也有所减轻。结论急性脑外伤后,脑组织NF-κB的表达明显增加,CCK-8可以通过抑制NF-κB的活性有效的减轻继发性炎性损害。Objective To investigate the effect of cholecystokinin-8( CCK-8) on the changes of Necular Factor Kappa B( NF-κB) activity in rats with acute traumatic brain injury.Methods Sixty adult Sprague-Dawley rats weighted250 g ~ 300 g were randomly divided into three groups:control group,trauma group and CCK-8 treatment group.The NF-κB activity was detected by electrophoretic mobility shift assay( EMSA) and the expression of NF-κB within cells was detected by immunohistochemistry,also the water content in brain tissue of injury part was measured by dry-wet weight method.Results Theactivity of NF-κB and water content in brain tissue in trauma group were significantly increased in different time points,as compared with those in control group,however,the NF-κB activity was obviously inhibited,moreover,the brain edema was alleviated at some extent in CCK-8 treatment group.Conclusion The activity of NF-κB in brain tissue is obviously increased immediately after acute traumatic brain injury,however,CCK-8 can effectively relieve the damage caused by secondary inflammatory reaction by inhibiting the activity of NF-κB.
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