【摘要】 目的:探讨脑组织中细胞间黏附分子-1(intercellular adhesion molecule-1,ICAM-1)和血管细胞黏附分子-1(vascular cell adhesion molecule-1,VCAM-1)在大鼠脑缺血损伤后不同时相不同脑区的表达及嘎日迪-13对其影响。方法:雄性SD大鼠360只,将大鼠随机分为假手术组、脑缺血模型组、嘎日迪-13大剂量组(240 mg/kg)、嘎日迪-13中剂量组(120 mg/kg)、嘎日迪-13小剂量组(60 mg/kg)5组,每组又随机分为缺血1h组、6 h组、12 h组、24 h组、72 h组与120 h组6个时相组,采用改良Zea Longa线栓法制备大鼠大脑中动脉栓塞模型,免疫组织化学法检测脑组织中ICAM-1和VCAM-1在1 h、6 h、12 h、24 h、72 h和120 h蛋白的表达。结果:与假手术组比较,模型组缺血侧海马、纹状体和大脑皮质区ICAM-1、VCAM-1阳性表达量显著升高,1 h后开始上升,24 h达高峰,之后逐渐下降(P<0.01),具有显著性差异。嘎日迪-13大、中、小剂量组缺血侧海马、纹状体和大脑皮质区可明显降低ICAM-1、VCAM-1的阳性表达量,与模型组比较具有显著性差异(P<0.01或P<0.05)。结论:嘎日迪-13可能是通过减少脑缺血损伤后各时相神经元的损伤,调节黏附分子相互之间的作用,抑制其合成、分泌及释放,来减轻脑组织损伤,从而发挥对脑缺血损伤的保护作用。更多还原

【Abstract】 Objective: To investigate the expressions of intercellular adhesion molecule-1(ICAM-1) and vascular cell adhesion molecule1(VCAM-1) in brain tissue at different phase at different encephalic region after cerebral ischemic in rats as well as the effect of Gridi-13 on them.Methods: A total of 360 male SD rats were selected.They were randomly divided into sham-operated group,model group,Gridi-13 large dose group,Gridi-13 middle dose group and Gridi-13 small dose group.Each group was randomly divided into 1 h,6 h,12 h,24 h,72 h and 120 h time phase groups.The middle cerebral artery occlusion(MCAO) model was established by modified Zea Longa thread-occlusion method and the contents of ICAM-1 and VCAM-1 in brain tissue were determined by Immunohistochemical method.Results: Compared with the sham group,model group’s ischemic hippocampus,striatum and cerebral cortex positive expressions of ICAM-1 and VCAM-1 were significantly increased,while rising after the cerebral ischemic injury for 1 h,reaching the peak at 24 h,and then going down gradually,with significant differences(P < 0.01).Garidi-13 in each dose group’s ischemic hippocampus,striatum and cerebral cortex can significantly reduce the protein expression levels of ICAM-1 and VCAM-1,and had significant difference compared with those of the model group(P < 0.01 or P <0.05).Conclusion: Gridi-13 may be related with alleviating neuronal damage,regulating adhesion molecule and relieving the injury of brain tissue to play a role of therapeutic action in cerebral ischemic injury.更多还原