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IL-17和ICAM-1在大鼠急性心肌缺血再灌注后无复流现象中的表达 被引量:6

Expression of interelenkin-17 and intercellular adhesion molecule-1 on noreflow phenomenon in acute myocardial infarction and reperfusion in rats
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摘要 目的探讨前炎症因子白介素-17(interelenkin-17,IL-17)与细胞间黏附因子-1(intercellular ad-hesion molecule-1,ICAM-1)在大鼠急性心肌缺血再灌注后无复流现象中的表达。方法 Wistar大鼠12只,随机分成2组:假手术组、损伤组,每组6只。损伤组给予冠状动脉结扎60 min、再灌注15 min,建立大鼠急性心肌缺血再灌注模型,假手术组只穿线不结扎。大鼠冠状动脉结扎前,结扎后15 min、30 min、45 min、再灌15 min时查心电图,再灌15 min时由股静脉注入硫磺素和Evans蓝,然后取血及心脏(只留左心室),将心脏沿长轴切成5~7片心肌,在365 nm光波下观察结扎区是否存在无荧光区域,即无复流区域。采用酶联免疫吸附法(enzyme linked immunosorbent assay,ELISA)测血清IL-17,免疫组化法测定ICAM-1。结果大鼠急性心肌缺血再灌注后存在无复流现象。与假手术组(49.75 pg/mL±14.06 pg/mL)相比,损伤组血清IL-17水平明显升高(151.6 7 pg/mL±11.19 pg/mL,P<0.01)。与假手术组大鼠心肌ICAM-1蛋白表达的IOD值(64.74±10.01)相比,损伤组非结扎区心肌ICAM-1蛋白表达的IOD值(67.35±11.57)差异无统计学意义(P>0.05),损伤组无复流区ICAM-1蛋白的IOD值(316.16±49.35)明显增加(P<0.01)。且IL-17和ICAM-1有相关性。结论 IL-17和ICAM-1参与大鼠急性心肌缺血再灌注后无复流现象的发生,且二者有相关性。推测IL-17的释放对ICAM-1的表达具有促进作用,从而促进无复流的发生、发展。 Objective To explore the expression of interelenkin-17(IL-17)and intercellular adhesion molecule-1(ICAM-1)on no-reflow phenomenon in acute myocardial infarction and reperfusion in rats.Methods Twelve healthy male Wistar rats were randomly divided into 2 groups:sham operation group(n=6),and injury group(n=6).The coronary artery of injury group rats were ligated for 60 min,then opened for 15 min to establish the acute myocardial ischemia-reperfusion model of rat.The sham operation group was only put seam through the coronary artery without ligation.The electrocardiogram was checked before ligated,ligated 15 min,30 min,45 min and reperfused 15 min.After reperfusion for 15 min,the thioflavine S and Evens were injected from femoral venous,then the heart and blood were obtained(keeping only left ventricular).Hearts were sliced transversely into five to seven sections.No-reflow phenomenon was observed after acute myocardial ischemia-reperfusion under the ultraviolet light(365 nm).The level of serum IL-17 was detected by enzyme linked immunosorbent assay(ELISA) method and the expression of ICAM-1 was measured by immunohistochemical method.Results No-reflow phenomenon was existed after acute myocardial ischemia-reperfusion.Compared with the sham group,the level of serum IL-17 of injury group was increased obviously[49.75 pg/mL±14.06 pg/mL vs 151.67 pg/mL±11.19 pg/mL,P0.01],the expression of ICAM-1 of myocardium in no-reflow area in injury group rats was increased obviously[64.74±10.01 vs 316.16±49.35,P0.01],but the expression of ICAM-1 of myocardium in no ligation region in injury group rats had no statistical significance.The level of ICAM-1 was related with the level of surm IL-17.Conclusion The IL-17 and ICAM-1 play an imporant role in no-reflow injury.IL-17 can reduce the expession of ICAM-1 that increase the inflammation and disfunction of the endothelial cell,then promote the no-reflow.
出处 《哈尔滨医科大学学报》 CAS 北大核心 2011年第5期401-404,408,共5页 Journal of Harbin Medical University
基金 黑龙江省攻关课题(GB07C32407) 哈尔滨医科大学附属第二医院博士课题基金(BS2007-03)
关键词 缺血再灌注 无复流 白介素-17 细胞间黏附因子-1 myocardial ischemia-reperfusion no-reflow interelenkin-17 intercellular adhesion molecule-1
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