摘要
目的:研究慢性应激对大鼠主动脉超微结构与热休克蛋白70(NSP70)表达的影响。方法:将雄性Wistar大鼠随机分为对照组11只和实验组12只。实验1￣21d,实验组接受各种不同的应激,单笼喂养。对照组群养,不给任何刺激。实验第22d取主动脉组织,透射电镜观察超微结构,免疫组化法检测热休克蛋白70(HSP70)表达。结果:实验组体质量明显下降,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。实验组大鼠主动脉组织出现明显的超微结构改变:部分内皮脱落,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。对照组主动脉超微结构基本正常。实验组主动脉HSP70表达高于对照组(P<0.05)。结论:慢性应激可引起主动脉细胞超微结构改变。引起主动脉HSP70表达增强。HSP70既是一种保护因素,也是机体正在经历应激损伤的标志。
Objective：To study the effects of chronic stress on the ultrastructure and expression of heat shock protein-70 （HSP70） in rat aorta. Methods：Male Wistar rats were randomly divided into experiment group （n = 12） and control group （n = 11）. The rats were fed separately and received various stimuli every day for 21 days in experiment group,and in control group the rats were fed together and received no stimulus. The rats were killed on day 22, and the aorta was sampled. The uhrastrocture of aorta was observed under transmission electron microscope,and the expression of HSP70 was detected by immunohistochemical method. Results：In experiment group,the body weight and the times of ambulation, rearing, and grooming significantly decreased, and the defecation and latency time significantly increased. The ultrastructural changes of the aorta, including desquamated endothelium and transformation of contractile phenotype to synthetic phenotype, migration into intima, and mitochondrial degeneration in smooth muscle cells, were found in experiment group. The ultrastructure of aorta was essentially normal in control group. The expression of HSP70 in experiment group was significantly higher than that in control group （P 〈 0.05 ）. Conclusion：Chronic stress could induce significant ultrastmctural changes and overexpression of HSP70 in rat aorta. HSP70 is a protective factor as well as a marker of lesion.
出处
《中国医科大学学报》
CAS
CSCD
北大核心
2007年第5期532-534,共3页
Journal of China Medical University
