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机构地区:[1]重庆医科大学附属第二医院神经内科,重庆400010
出 处:《重庆医科大学学报》2008年第3期329-330,340,共3页Journal of Chongqing Medical University
摘 要:目的:探讨NF-κB在大鼠脑缺血再灌注后炎性反应中的作用。方法:制备脑缺血再灌注模型。24h后,免疫组化检测假手术组、模型组和干预组中NF-κB p65的表达,测定脑组织匀浆中性粒细胞趋化因子(CINC)含量变化,同时观察海马CA1区病理组织学改变。结果:模型组大鼠脑组织的NF-κB p65阳性表达和CINC含量与假手术组相比明显增高,P<0.05;干预组大鼠脑组织的NF-κB p65阳性表达和CINC含量与模型组相比明显受抑制,P<0.05。干预组脑组织病理改变较模型组轻。结论:NF-κB参与了脑缺血再灌注后炎性反应中前炎性因子的调控过程。Objective:To investigate the role of nuclear factor-κB (NF-κB) in rats with cerebral ischemia-reperfusion injury. Methods:Rat models of cerebral ischemia-reperfusion were established. 24hours later, the expression of NF-κB in rat brain of sham-operation group,operation group and intervention group was detected with immunohistochemistry method,Cytokin-induced neutrophil chemotactics(CINC) in rat brain were measured and histopathological examinations were conducted on the hippocampal CA1. Results:The expression of NF-κB p65 and CINC in the operation group increased significantly compared with the sham-operation group(P〈0.05). But the expression of NF-κB p65 and CINC in the intervention group were inhibited significantly compared with the operation group(P〈0.05 ).The pathological changes of the intervention group were slighter than those of the operation group. Conclusion:The results suggest that NF-κB may play an important role in the release of inflammation factors and gathering of inflammation cells induced by ischemia-reperfusion injury.
分 类 号:R743.31[医药卫生—神经病学与精神病学]
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