大鼠心肌缺血再灌注损伤与热休克蛋白72的保护作用  

Effects of heat shock protein 72 in protecting myocardium of rats with ischemia reperfusion injury

作　　者：张伟[1] 王明荣[1] 杨宗诚[2] 

机构地区：[1]解放军第三军医大学西南医院心胸外科,重庆市400038 [2]解放军第三军医大学西南医院烧伤研究所,重庆市400038

出　　处：《中国临床康复》2004年第27期5826-5827,共2页Chinese Journal of Clinical Rehabilitation

摘　　要：目的:观察热休克反应(heatshockresponse,HSR)后0、24、48、96、192h热休克蛋白72(heatshockprotein72,HSP72)表达水平的变化及再灌注后心肌组织超氧化物歧化酶(superoxidedismutase,SOD)含量、心肌收缩功能变化,探讨HSP72对缺血再灌注心肌保护的可能机制。方法:Wistar大鼠48只,体质量250～300g,雌雄不均,随机分为6组,每组8只。全身高温42℃维持15min制作热休克模型。各组心脏离体逆行灌注,常温下(37℃)缺血25min,再灌注40min。测定缺血前、再灌注后心肌组织SOD含量,心肌收缩功能,观察各组心肌HSP72表达。结果:实验组再灌注后24h和48h心肌组织SOD活性分别为(22.37±4.75)、(23.39±4.86)Nu/mg,明显高于对照组。对照组和热预处理后0h几乎无HSP72表达(面密度),其表达高峰在热预处理后24,48h,分别为137.89±25.25,146.09±28.34,随后逐渐降低,于192h返回基线水平。HSP72表达与再灌注后心肌组织SOD(r=0.9234),心功能恢复率LVSP(r=0.9012)呈显著正相关(P<0.05).结论:热休克蛋白能提高抗氧化酶活性,减轻心肌缺血再灌注损伤。AIM:To observe the changes of heat shock protein 72(HSP72) expression 0, 24,48,96 and 192 hours after heat shock response(HSR) and the variations of myocardial super oxide dismutase(SOD) content and the myocardial systolic function,so as to explore the possible mechanism of HSP for protecting ischemia reperfusion myocardium. METHODS :Forty eight Wistar rats (male and female),weighing 250-300 g,were randomly divided into six groups of 8 rats in each.Models of heat shock were established by maintaining the temperature of the whole body at 42 ℃for 15 minutes.The hearts were perfused reversely in vitro in all the groups at the normal temperature(37 ℃) for 25 minute ischemia and 40 minute reperfusion.The SOD content in myocardial tissue, myocardial systolic function were detected before ischemia and after reperfusion,and the myocardial HSP72 expressions in all the groups were observed. RESULTS:The content of myocardial SOD at 24 and 48 hours after reperfusion in the experimental group were(22.37±4.75) and(23.39±4.86) Nu/mg,significantly higher than those in the control group.Nearly no HSP72 expression(surface density) was observed 0 hour after hyperthermia and in the control group,and its peak value appeared at 24 and 48 hours after hyperthermia(137.89±25.25 and 146.09±28.34),and then decreased gradually,and returned to the basal level at 192 hours after hyperthermia.The HSP72 expression had significant positive correlation with SOD activity in cardiac tissue(r=0.923 4) and recovery rate of cardiac function (r=0.901 2)(P< 0.05). CONCLUSION:HSP72 can increase the antioxidant enzyme activity,and reduce the myocardial ischemia reperfusion injury.

关 键 词：热休克反应 热休克蛋白72 再灌注损伤 

分 类 号：R542.2[医药卫生—心血管疾病]