心肌缺血再灌注损伤与白细胞介素-1表达水平的相关性研究(英文)

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背景:近年来白细胞介素-1(IL-1)与心肌缺血再灌注损伤(myocardialischemicalreperfusioninjury,MIRI)之间的关系引起了人们的关注,但其确切作用点及作用机制仍不清楚,阐明他们之间的内在关系有重要理论价值。目的:研究IL-1mRNA及蛋白在缺血心肌的表达规律及与再灌注损伤之间的关系,并观察N-乙酰半胱氨酸(N-acetylcysteine,NAC)对缺血组织的影响。设计:随机对照的实验研究。地点、材料和干预:本实验在解放军第三军医大学中心实验室完成。实验选用Wistar大鼠116只,随机单盲分设缺血再灌注(ischemiareperfu-sion,IR)组(IR组),IR+NAC治疗组和假手术对照组;先缺血60min,然后分设再灌注1,3,6,12,24h共5个时相点;治疗组于缺血10min腹腔注射NAC160mg/kg。于各相应时相点活杀动物取缺血区心肌待测。观察缺血心肌组织IL-1mRNA、蛋白表达水平、自由基系统、ATP酶活性及心肌梗死范围变化。IL-1mRNA表达用原位杂交检测,用免疫组织化学法测定其蛋白表达,心肌组织丙二醛用硫代巴比妥酸比色法测定,心肌组织超氧化物歧化酶(superoxidedismutase,SOD)活性测定用黄嘌呤过氧化物酶法,心肌组织ATP酶活性用磷比色法测定,心肌梗死范围测定用氯化三苯基四氮唑(triphenyltetrazoliumchloride,TTC)染色法。主要观察指标:①心肌IR时 BACKGROUND: The relationship between interleukin-1 (IL-1) and myocardial ischemia-reperfusion injury (MIRI) has drawn people’s attention in recent years. However, its exact site of action and its mechanism of action remain unclear. The intrinsic relationship between the important theoretical value. OBJECTIVE: To investigate the expression of IL-1 mRNA and protein in ischemic myocardium and its relationship with reperfusion injury and to observe the effect of N-acetylcysteine ​​(NAC) on ischemic tissue. Design: Randomized controlled experimental study. Location, Materials and Intervention: This experiment was completed at the Central Laboratory of the Third Military Medical University of PLA. One hundred and sixty-six Wistar rats were randomly divided into three groups: ischemiareperfusion group (IR group), IR + NAC group and sham operation group , 3,6,12,24h total of 5 time points; the treatment group in the ischemic 10min intraperitoneal injection of NAC160mg / kg. At the appropriate time point to kill animals take ischemic myocardium to be tested. The changes of IL-1mRNA, protein expression, free radical system, ATPase activity and infarct size in ischemic myocardium were observed. The expression of IL-1mRNA was detected by in situ hybridization. The protein expression of IL-1mRNA was detected by immunohistochemical method. The content of malondialdehyde in myocardium was measured by thiobarbituric acid colorimetric assay. The activity of superoxide dismutase (SOD) Determination of xanthine peroxidase method, myocardial ATPase activity was determined by phosphorus colorimetric determination of myocardial infarction range with triphenyltetrazolium chloride (triphenyltetrazolium chloride, TTC) staining. MAIN OUTCOME MEASURES: ① myocardial IR
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