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

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。

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

Objective To determine the expression of interleukin-1,8 and 10 in different time after myocardial ischemia reperfusion injury(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-cardiomyocytes 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.Conclusion (1)Inflammatory response caused principally by neutrophilic 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.