嘎日迪-13对大鼠脑缺血后不同时相不同脑区ICAM-1、VCAM-1表达的影响

被引:12
作者
曹丽霞
郑延泽
武海军
何静波
田彩云
张浩楠
覃建民
徐继辉
杨玉梅
机构
[1] 包头医学院心血管研究室
关键词
嘎日迪-13; 脑缺血; ICAM-1; VCAM-1;
D O I
暂无
中图分类号
R29 [中国少数民族医学];
学科分类号
100513 [民族医学];
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。
引用
收藏
页码:3009 / 3014
页数:6
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