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目的观察慢性脑缺血大鼠海马CA1区神经元核因子-κBp65(nuclear-κBp65,NF-κB p65)、ICAM-1的表达,探讨丁基苯酞(DBT)在慢性脑缺血中的作用。方法采用双侧颈总动脉持久性结扎(2-VO)制备慢性脑缺血模型,同时设立对照组及丁基苯酞低剂量及高剂量治疗组。采用光镜大鼠海马CA1区组织形态学变化;采用免疫组织化学方法检测NF-κBp65及ICAM-1的表达。结果与对照组相比,模型组海马CA1区神经元严重受损,NF-κBp65、ICAM-1显著升高(P<0.01),丁基苯酞治疗后,海马区形态学明显改善,海马CA1区NF-κBp65、ICAM-1表达明显减少(P<0.01)。结论丁基苯酞可能通过减少慢性脑缺血大鼠NF-κBp65、ICAM-1在海马神经元中的表达,减轻神经元变性、坏死,抑制炎症反应,从而减轻慢性脑缺血大鼠的脑损伤。
Objective To investigate the expression of nuclear factor-κB p65 (NF-κB p65) and ICAM-1 in the hippocampal CA1 subfield in chronic cerebral hypoperfusion rats and to explore the role of butylphthalide (DBT) in chronic cerebral ischemia . Methods The model of chronic cerebral ischemia was established by permanent bilateral carotid artery ligation (2-VO). At the same time, the control group and the butylphthalide treatment group were given low dose and high dose. The histopathological changes of hippocampal CA1 region were observed with light microscope. The expressions of NF-κBp65 and ICAM-1 were detected by immunohistochemistry. Results Compared with the control group, the neurons in the hippocampal CA1 region of the model group were severely damaged and the expressions of NF-κBp65 and ICAM-1 were significantly increased (P <0.01). After the treatment with butylphthalide, the morphology of the hippocampus was significantly improved. The hippocampal CA1 The expression of NF-κBp65 and ICAM-1 was significantly decreased (P <0.01). Conclusion Butylphthalide may reduce the neuronal degeneration, necrosis and inflammation by decreasing the expression of NF-κBp65 and ICAM-1 in hippocampal neurons in rats with chronic cerebral ischemia damage.