丁基苯酞对血管性痴呆大鼠的保护作用

Protective effects of butylphthalide on ischemic vascular dementia in rats

目的研究丁基苯酞(buty lphthalide,DBT)对血管性痴呆大鼠学习记忆、核因子-κB(nuclear factor-κB,NF-κB)及环氧合酶-2(cyclooxygenase-2,COX-2)的影响,探讨DBT对血管性痴呆的干预疗效。方法大鼠随机分为假手术组(SOG)、模型组(MG)、丁基苯酞大剂量治疗组(DBT1)、丁基苯酞小剂量治疗组(DBT2)、丁基苯酞预防组(DBT3),用药1月,采用HE染色,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。结果与模型组比较,DBT不同剂量治疗1月后,学习记忆能力改善,海马CA1区神经元变性、坏死不同程度减轻;NF-κBp65、COX-2阳性细胞数表达减少(P<0.01),且不同剂量组间亦有差异(P<0.01)。结论丁基苯酞改善实验大鼠的学习记忆能力,减少实验大鼠海马CA1区神经细胞的丢失,降低血管性痴呆大鼠海马CA1区NF-κB、COX-2表达,可能具有预防和治疗血管性痴呆的作用。

Objective To observe the effects of butylphthalide（DBT）on learning-memory ability and expression of nuclear factor-κB（NF-κB） and cyclooxygenase-2（COX-2）,and investigate its curative effect on the intervention of vascular dementia（VD）.Methods Rats were classified into five groups randomly,model group（MG）,DBT high dose group（DBT1）,DBT low dose group（DBT2）,DBT precautious against group（DBT3）and sham operation group（SOG）.The treatment lasted for one month.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 In drug-treated groups,DBT improved the performance of learning and memory of VD rats in Morris water maze,attenuated the pathological alterations of pyramidal layer in the hippocampal CA1 area,decreased the expression of NF-κBp65 and COX-2（P〈0.01）,the difference of each group was apparent（P〈0.01）.Conclusion The results suggest DBT can improve the learning-memory ability of VD rats,protecte neurons in the hippocampal CA1 area,decrease the expression of NF-κBp65 and COX-2.DBT may have the effects to protect and treat vascular dementia.