白介素-1、8、10与药物干预对大鼠心肌缺血再灌注损伤的影响  

Effect of interleukin-1,8,10 and medicine precondition on yocardial ischemia reperfusion injury in rats

作　　者：张艳芳[1] 王琦[2] 杨廷桐[3] 

机构地区：[1]新乡医学院生物化学教研室,河南新乡453003 [2]河南中医学院组织胚胎学教研室,河南郑州450008 [3]新乡医学院形态学实验室,河南新乡453003

出　　处：《新乡医学院学报》2006年第6期572-574,F0003,共4页Journal of Xinxiang Medical University

摘　　要：目的检测白介素-1、8、10在心肌缺血再灌注损伤(MIRI)不同时段的表达,探讨其作用机制及对MIRI的影响。方法70只大鼠随机分为3组:假手术组(对照组,n=10),缺血再灌注组(模型组,n=30)和甲泼尼龙治疗组(药物组,n=30)。后两组再分设缺血0.5h、再灌注2h、4h、8h、12h和24h共6个亚组。建立大鼠MIRI模型,观察缺血再灌注(IR)损伤心肌的形态学变化,检测血清中白介素-1(IL-1)、白介素-8(IL-8)、白介素-10(IL-10)的动态表达。结果(1)缺血再灌注后HE染色见心肌细胞间大量炎细胞浸润,并呈明显缺血、坏死性改变,随病程不同表现程度有所差异。(2)模型组与药物组的血清IL-1、IL-8和IL-10浓度均较对照组明显升高(P<0.05)。IL-1高峰出现于IR4h,IL-8峰值在IR8h;药物组较模型组同时相点IL-1、IL-8均降低(P<0.05)。血清IL-10在模型组于IR12h达高峰,药物组较模型组表现为峰值提前到IR8h。结论(1)以中性粒细胞浸润为主的炎症反应是导致MIRI的重要原因之一;(2)IL-1和IL-8对心肌有致损作用,而IL-10则具心肌保护作用;(3)甲泼尼龙预处理有保护缺血心肌的作用。Objective To determine the expression of interleukin-1,8 and 10 in different time after myocardial ischemia reperfusion inj ury（MIRI）, and to investigate thire possible mechanism and effect on ischemia reperfusion （IR） injury. Methods A total of 70 rats were randomly divided into 3 groups： sham operation group（control group, n = 10）, IR group（model group, n = 30）, methylpre- dnisolone-treated group（ administration group, n = 30）, and the later 2 groups were observed at 0.5 h after ischemia and 2,4,8,12 and 24 h after reperfusion. The rat model of MIRI was established,and the relationship of IR myocardial tissue and the levels of serum IL-1,8 and 10 was analized. Results （1）HE staining showed masses of inflamematory cells inter-cardiomyoeytes after IR. （2）Compared with control group, IL-1,8 and 10 in model group and administration group obviously increased（P〈 0.05）;The peak value of IL-1 at IR 4h, and IL-8 at IR 8h; IL-1 and IL-8 in administration group were lower than those of model group（ P〈 0.05）. Compared with model group（peak value at IR 12h）, the peak value of IL-10 in administration group was advanced to IR 8h. Conelusion （ 1 ） Inflammatory response caused principally by neutmphilic infiltration is one of the important reason of MIRI. （2）In the process of MIRI, IL-1 and IL-8 may cause myocardial injury,but IL- 10 has myocardial protective effect. （3）Precondition with methylprednisolone may protect ischemial myocardial tissue.

关 键 词：心肌缺血再灌注损伤 炎症反应 白介素 甲泼尼龙 

分 类 号：R96[医药卫生—药理学]