主动脉超微结构和细胞间黏附分子1在慢性强迫游泳应激大鼠模型的表达

Ultrastructure and intercellular adhesion molecule-1 expression in the aorta of rat models following chronic forced swimming stress

目的:观察主动脉超微结构改变和主动脉细胞间黏附分子1在慢性强迫游泳应激模型大鼠体内的表达特点,为应激增加心血管系统疾病危险性的研究机制提供新的依据。方法:实验于2005-07/10在中国医科大学生理实验室完成。①实验分组:将26只健康青年雄性Wistar大鼠随机分成实验组和对照组各13只。②实验方法:实验第1～21天,每天上午8:00将大鼠置于水温4℃,水深为30cm的水池中强迫其游泳,每次游5min,1次/d。对照组不给予任何刺激。③实验评估:实验第22天各组大鼠麻醉后断头处死,处死前再次测定行为并称质量。透射电镜观察大鼠主动脉超微结构改变;采用免疫组化ABC法检测主动脉细胞间黏附分子1表达情况。结果:26只大鼠均进入结果分析。①开场实验结果及体质量:经过21d应激,实验组大鼠体质量明显下降,水平穿越格数、直立次数、修饰次数减少,粪便粒数、中央格停留时间增加。②主动脉超微结构:实验组大鼠主动脉组织部分内皮细胞脱落,平滑肌细胞由收缩表型向合成表型转化,向内膜迁移,线粒体变性,对照组大鼠主动脉超微结构基本正常。③主动脉组织细胞间黏附分子1表达:实验组主动脉组织细胞间黏附分子1表达增强,显著高于对照组(11.35±5.41,22.85±5.71,t=5.06,P<0.01)。结论:慢性强迫游泳应激可以导致大鼠主动脉超微结构发生改变,主动脉细胞间黏附分子1的表达增强,慢性强迫游泳应激所致主动脉血管内皮细胞损伤可能和炎症反应有关。

AIM： To study the effects of chronic forced swimming stress on ultrastructure and the expressive changes of intercellular adhesion molecule-1 （ICAM-1） in aorta of rats and provide new evidences for research on stress-induced risk of disease of cardiovascular system. METHODS： The experiment was performed at Laboratory of Physiology of China Medical University from July to October 2005. ①Totally 26 healthy male young Wistar rats were randomly divided into experimental group and control group with 13 in each group. ②From 1 to 21 days, rats in the experimental group received forced swimming stress at eight o＇clock in the moming at 4 % in 30 cm-depth pool, once 5 minutes in one day. Rats in the control group did not receive any stress. ③On the 22nd day all the rats were determined in behavior and weighted and then killed after anaesthetizing. Ultrastructure in aorta of rats was observed under transmission electron microscope. The expression of ICAM-1 protein in aorta was determined by immunohistochemical ABC method. RESULTS： Totally 26 rats were involved in the result analysis. ①After 21-day stress, body mass, ambulation, rearing and grooming decreased and stopping time in center, defecation increased in rats of the experimental group. ②Smooth muscle cell （SMC） happened transform from contracted phenotype to synthesis phenotype, migration and mitochondrion degeneration, some endothelium cells were lost in rats of the experimental group. The ultrastructure in rats of the control group was essentially normal. ③ICAM-1 expressed obviously in aorta of rats of the experimental group, and the expression of ICAM-1 was obviously higher than those in the control group （11.35±5.41,22.85±5.71 ,t = 5.06,P 〈 0.01）. CONCLUSION： The chronic forced swimming stress can exchange the ultrastructure in aorta of rats. The chronic forced swimming stress can lead to the more expression of ICAM-1 in aorta. The damage of endothelium cells in aorta is associated with inflammatory process.