论文部分内容阅读
目的检测慢性脑缺血老龄大鼠核因子-κB(nuclear factor κB,NF-κB)、环氧合酶-2(cyclooxygenase-2,COX-2)的表达,探讨丁基苯酞(DBT)在慢性脑缺血中的抗炎作用。方法健康Wistar大鼠60只,按随机数字表分为4组,分别为对照组、模型组、缺血高剂量DBT组、缺血低剂量DBT组,每组15只。采用光镜及免疫组织化学方法对各组大鼠海马CA1区及颞叶皮层组织形态学、NF-κB及COX-2的表达进行检测。结果与模型组比较,丁基苯酞不同剂量治疗1个月后,大鼠海马CA1区及颞叶皮层神经元变性、坏死不同程度减轻;NF-κB p65、COX-2阳性细胞数表达减少(P<0.01),高低剂量组阳性细胞数差异有统计学意义(P<0.01)。结论丁基苯酞可以减轻慢性脑缺血老龄大鼠神经元变性、坏死;减少NF-κB p65、COX-2的表达,可能是丁基苯酞抑制炎症反应的途径之一。
Objective To detect the expression of nuclear factor κB (NF-κB) and cyclooxygenase-2 (COX-2) in the aged rats with chronic cerebral ischemia and to investigate the effect of butylphthalide (DBT) Anti-inflammatory effects in chronic cerebral ischemia. Methods Sixty healthy Wistar rats were randomly divided into four groups according to random number table: control group, model group, high dose of DBT group and low dose of DBT group (n = 15). The morphological changes, the expressions of NF-κB and COX-2 in the hippocampal CA1 and temporal cortex were detected by light microscopy and immunohistochemistry. Results Compared with model group, the denaturation and necrosis of hippocampal CA1 area and temporal cortex neurons were alleviated in different degrees after butylphthalide treatment for 1 month. The expression of NF-κB p65 and COX-2 positive cells decreased P <0.01). There were significant differences in the number of positive cells between the high and low dose groups (P <0.01). Conclusion Butylphthalide can reduce neuronal degeneration and necrosis in aged rats with chronic cerebral ischemia and reduce the expression of NF-κB p65 and COX-2, which may be one of the ways of butylphthalide inhibiting inflammation.