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

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-κB p65,NF-κBp65)与环氧合酶-2(cyclooxygenase-2,COX-2)的表达,探讨NF-κB、COX-2对VD大鼠的损伤作用。方法28只大鼠随机分为两组,假手术(SOG)组(n=13)和模型(VD)组(n=15),采用HE染色,光镜下观察海马CA1区锥体细胞的改变,免疫组化方法检测海马CA1区NF-κBp65、COX-2蛋白的表达。结果与假手术组相比,模型组组海马CA1区锥体细胞损伤、丧失明显,NF-κBp65、COX-2蛋白表达高于假手术组,与假手术组相比有统计学意义(P(0.01)。结论血管性痴呆大鼠海马CA1区NF-κBp65、COX-2蛋白的表达增加,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 rule of nuclear factor-κB p65 （NF-KBp65） and cyclooxygenase-2 （COX-2） in the formation of vascular dementia（VD） and investigate the possible pathogenesis of VD. Methods 28 Wistar rats were distributed into two groups randomly, experimental group, 15 Wistar rats, the sham-operated group（ SOG）, 13 rats. Rats of experimental group were treated with a permanent bilateral common carotid arteries （CCA） occlusion （2-VO） to establish vascular dementia model. Rats were evaluated on learning-memory ability by Morris water maze test. The chan- ges 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 hippocampus in VD group. In VD group, the expression of NF- κBp65 and COX-2 in hippocampal CA1 region was more obvious（P 〈 0.01 ）. Conclusion Chronic cerebral hypoperfu- sion contribute to the formation of VD, and NF-κBp65 and COX-2 may play an injury role in learning-memory ability disorder.