摘要
目的:热休克蛋白是细胞在应激条件下产生的一类高度保守的蛋白质,它可以从抵抗损伤和加速修复两个方面对细胞进行保护。研究表明热休克蛋白对心肌缺血再灌注损伤有内源性的抵抗作用。本文对热休克蛋白及其内源性抵抗心肌缺血再灌注损伤的作用机制进行综述。资料来源:①从图书馆手工查阅相关领域的学术期刊,重点是核心期刊,查阅有关心肌损伤与热休克蛋白之间关系的文献,关键词为“心肌损伤、热休克蛋白、缺血再灌注”。②在cnki数据库及PubMed检索2000/2006心肌缺血再灌注损伤保护方面的文献资料,关键词是“心肌损伤、热休克蛋白”。资料选择:手工和应用计算机分别检索到13篇和29篇与热休克蛋白与心肌缺血再灌注损伤有关的文献。纳入标准:选择实验性文献,即一次性文献。对于内容相近的文献选择在核心期刊发表或年限较近的文章。排除标准:重复性研究。资料提炼:共得到35篇文献,其中2004/2006的文献有14篇,2000/2003的文献7篇。资料综合:热休克蛋白是细胞在应激情况下启动热休克基因从而产生的一种结构高度保守的蛋白质,几乎存在于从原核生物到真核生物的所有生物体。它具有非特异性、高度保守性、热休克蛋白70表达突出性、时间性、弱的ATP酶的活性和交叉耐受性等特性。热休克蛋白对细胞具有保护作用,主要表现在抵抗损伤和加速修复这两方面。20世纪80年代末,人们开始注意到热休克蛋白具有心肌保护作用,1988年,Currie等将SD大鼠进行热休克预处理,待其恢复24h后,进行离体心肌缺血再灌注,结果发现热休克组大鼠心肌缺血再灌注损伤后力学指标的恢复明显改善,心肌超微结构的损伤也有不同程度的减轻。热休克蛋白抵抗心肌缺血再灌注损伤的机制包括:稳定细胞内变性的蛋白质;减轻细胞内的离子紊乱;保护血管内皮细胞的功能;干扰应激所启动的细胞调亡程序等4个方面。结论:热休克蛋白对心肌缺血再灌注损伤具有内源性的抵抗作用。
OBJECTIVE： Hot shock protein （HSP） as a kind of highly conservative protein is generated from cells under stress. It could protect cells through resisting injury and accelerating repair. Recent researches show that HSP displays the function of endogenous resistance to myocardial ischemia/reperfusion injury. In this paper, we reviewed the mechanism of HSP and its endogenous resistance to myocardial ischemia/reperfusion injury. DATA SOURCES： The articles about the association between myocardial ischemia/reperfusion injury and HSP were searched manually from the library among the academic journals, especially the core journals with the key words of ＂myocardial injury, heat shock protein, ischemia/reperfusion＂. Meanwhile, we searched CNKI and PubMed for articles about the protection of myocardial ischemia/reperfusion injury published between 2004 and 2006 with the key words of ＂myocardial injury, heat shock protein＂. STUDY SELECTION： Thirteen and twenty-nine articles about the association between myocardial ischemia/reperfusion injury and HSP were collected from the library and the Internet, respectively. Inclusive criteria： Experimental articles, namely primary document, and those published in core journals or in recent years. Exclusive criteria： Repetitive studies. DATA EXTRACTION： Totally 35 articles were collected, of which 14 were published between 2004 and 2006, and 7 between 2000 and 2003. DATA SYNTHESIS： HSP, a kind of protein with highly conservative structure, is generated from cells under stress; it is nearly found in all living bodies from prokaryote to eukaryote. HSP is characterized by non-specificity, highly conservation, obviously HSP-70 expressions, time manner, weak ATPase activity and cross resistance. HSP displays a protection to cells in resisting injury and accelerate repair. People did not pay attention to the protective effect of HSP on myocardium until the end of 1980＇s. In 1988, Currie et al treated the SD rats by HSP preconditioning. After twenty-four hours rest, the rats underwent myocardial ischemia/reperfusion injury, in which the mechanic index of the HSP group was improved significantly after myocardial ischemia/reperfusion injury, and the myocardial ultrastructural injury was lessened. The mechanisms of HSP to protect myocardial ischemia/reperfusion injury include stabling the degenerative protein in cell, lessening ionic disorder in cell, protecting the function of vascular endothelial cell and interfering cell apoptosis induced by stress. CONCLUSION： HSP shows the function of endogenous resistance to myocardial ischemia/reperfusion injury.
出处
《中国组织工程研究与临床康复》
CAS
CSCD
北大核心
2007年第21期4217-4220,共4页
Journal of Clinical Rehabilitative Tissue Engineering Research
