老年大鼠心肌缺血再灌注损伤时氧自由基与细胞间粘附分子-1的变化规律

Experimental study of the change of ICAM-1 and OFR in old rats after myocardial ischemic reperfusion

目的 探讨老年大鼠心肌缺血再灌注损伤 (IRI)时氧自由基 (OFR)与细胞间粘附分子 - 1 (ICAM -1 )的变化及其相互关系。方法 Wistar大鼠 1 1 2只 ,制作心肌IRI模型 ,设青、老年组 ;各组分设缺血 1小时 ,再灌注 3、 6、 1 2和 2 4小时时相点 ,用免疫组化法测ICAM - 1蛋白表达水平 ,用酶法测定中性粒细胞 (PMNs)浸润数 ,用硫代巴比妥酸比色法测定心肌组织丙二醛 (MDA) ,用黄嘌呤过氧化物酶法测定超氧化物歧化酶 (SOD)活性 ,TTC染色法测定梗死范围。结果 心肌IR时 ,青、老年组ICAM - 1蛋白质表达、PMNs浸润、心肌梗死范围、MDA含量均明显增高 ,SOD活性显著降低。但MDA、SOD达峰、谷值的时间早于ICAM - 1表达及PMNs浸润的峰值。这些指标老年组变化更明显。结论 心肌缺血再灌注时 ,OFR的增加促进了ICAM - 1表达的上调 ,继之激活PMN ,产生大量的OFR使心肌损伤加重。这种变化在老年大鼠中表现尤为显著 。

Objective To observe the relationship between the change of intercellular adhesion molecule-1(ICAM-1) and oxygen free radicals(OFR) on myocardial ischemic reperfusion(IRI) in old rats.Methods 112 rats were divided into young and old groups.The ischemic myocardial samples were observed in 1 hour after ischemia and 3,6,12,24 hours after IR.The myocardial levels of expression of ICAM-1 protein were evaluated by method of immunocytochemistry.The content of infiltration of polymorphonuclear neutrophils(PMNs),malomdialdehyde(MDA),superoxides dismutase(SOD) and the myocardial infarction area were measured,too.Results After IR,myocardial levels of expression of ICAM-1,MDA and PMNs were increased significantly;SOD was decreased significantly.In young group,although the indicators were increased after IR,the levels of increase were more significantly modification while comparing with old group.The curves′ peak and bottom points of MDA and SOD attached were earlier than ICAM-1 and PMNs reached respectively.Conclusion The increase of OFR leaded to ICAM-1 upregulation.ICAM-1 mediated PMNs adhesion and infiltration endothelial and myocardial cells.Subsequently,adherent,activated PMNs become the major source of OFRs,thereby contributing to tissue damage.The serious myocardial IRI might be caused by the high expression level of ICAM-1 in old rats.