血管性痴呆大鼠海马区核因子-κB、环氧合酶-2的表达变化  

Expression of nuclear factor-κB and Cyclooxygenase-2 in the hippocampus of rats with vascular dementia

作　　者：翟锴华[1] 卢宏[1] 腾军放[1] 王兴萍[1] 

机构地区：[1]郑州大学第一附属医院神经内科,郑州450052

出　　处：《中国实用神经疾病杂志》2007年第3期88-89,共2页Chinese Journal of Practical Nervous Diseases

摘　　要：目的通过检测血管性痴呆(vascular dementia,VD)大鼠海马CA1区核因子-κBp65(nuclear factor-κBp65,NF-κBp65)与环氧合酶-2(cyclooxygenase-2,COX-2)的表达,探讨NF-κB和COX-2的损伤作用。方法28只大鼠随机分为假手术组(SOG)13只和模型组(VD)15只,取海马CA1区为观察部位,HE染色观察锥体细胞的改变,免疫组化检测NF-κBp65、COX-2的表达。结果与SOG相比,VD大鼠海马CA1区锥体细胞损伤、丧失明显,NF-κBp65、COX-2蛋白增加,差异有统计学意义(P(0·01)。结论VD大鼠海马CA1区NF-κBp65、COX-2蛋白的高表达可能是学习记忆障碍的原因之一。Objective To observe the expression of nuclear factor-κB p65 （NF-κBp65） and cyclooxygenase-2（COX-2） in the hippocampal CA1 region and investigate the possible pathogenesis of vascular dementia （VD） . Methods 28 Wistar rats were distributed into two groups randomly, experimental group （VD） used 15 Wistar rats, the shamoperated group （SOG） were 13 rats. Rats of VD were treated with a permanent bilateral common carotid arteries occlusion （2-VO）. The changes of cell morphology in hippocampal CA1 area were detected by HE stain; the expression of NF-κBp65 and COX-2 in hippocampal CA1 region were measured by immunohistochemical assay method. Results By comparison with SOG, pyramidal cells on CA1 field were denaturalization and pyknosis in hippocampal CA1 region, the increase of NF-κBp65 and COX-2 in hippocampal CA1 region were obvious（P 〈 0.01）. Conclusion In hippocampal CA1 region of rats with VD, the increased NF-κBp65 and COX-2 may play an injury role in learning-memory ability disorder.

关 键 词：血管性痴呆 核因子-ΚBP65 环氧合酶-2 

分 类 号：R651.15[医药卫生—外科学]