中文摘要：

目的：研究核转录因子锌指蛋白580（ZFP580）在大鼠心肌缺血-再灌注（I-R）损伤中表达的变化,探讨其可能的作用。方法：48只SD大鼠分为：（1）假手术组;（2）I-R组,结扎冠状动脉左前降支30 min后恢复血液灌注;（3）L-精氨酸（L-Arg）预处理＋I-R组,于缺血前给予L-Arg 300 mg/kg,重复I-R组操作;（4）L-Arg预处理＋sham组。（2）、（3）组于I-R后1 h或4 h处死动物。各组大鼠取心肌标本HE染色,光镜下计数心肌组织中中性粒细胞数。检测血清中乳酸脱氢酶（LDH）、肌酸激酶（CK）活性及肿瘤坏死因子-α（TNF-α）浓度,半定量RT-PCR或免疫组化染色分析ZFP580及内皮型一氧化氮合酶（eNOS）在心肌细胞的表达。结果：I-R后,缺血区心肌细胞肿胀,周围大量中性粒细胞浸润,血清LDH、CK活性及TNF-α浓度升高,心肌ZFP580和eNOS表达下调（P〈0.05）。应用L-Arg预处理＋I-R后,血清LDH、CK活性及TNF-α浓度降低,心肌ZFP580和eNOS的表达回升。结论：心肌I-R损伤引起ZFP580表达下调。ZFP580及eNOS的表达上调可能是L-Arg预处理拮抗心肌I-R损伤的机制之一。

英文摘要：

AIM：To investigate the expression of transcription factor zinc finger protein 580（ZFP580） in the process of rat myocardial ischemia-reperfusion（I-R） injury with or without L-arginine preconditioning.METHODS： Forty-eight SD rats were randomly divided into sham group,I-R group,L-arginine preconditioning＋I-R group and L-arginine preconditioning＋sham group.Myocardial ischemia was induced by the ligation of left anterior descending coronary artery,and the rats were subjected to transient ischemia for 30 min followed by reperfusion for 1 h or 4 h.L-arginine was administered before ischemia in preconditioning groups.The cardiac histological changes were assessed by hematoxylineosin（HE） staining.The serum content of TNF-α and the activity of creatine kinase（CK） and lactate dehydrogenase（LDH） were detected.The expression of ZFP580 and endothelial nitric oxide synthase（eNOS） in the heart were measured by RTPCR and immunohistochemical analysis.RESULTS： Histological analysis showed that there were more polymorphonuclear neutrophils infiltrating in ischemic myocardium after reperfusion.Serum level of TNF-α and the activity of CK and LDH were significantly increased in I-R group,accompanying the down-regulation of ZFP580 and eNOS in the heart（P0.05）.L-arginine preconditioning up-regulated ZFP580 and eNOS in the heart,and decreased TNF-α level,CK and LDH activity in serum.CONCLUSION： Ischemia-reperfusion injury coincides with the down-regulation of ZFP580 and eNOS in the heart.The beneficial effects of L-arginine are partly mediated by up-regulating the expression of ZFP580 and eNOS.