中文摘要：

目的：探讨Ⅰ型多聚ADP核糖合成酶（PARP1）在心肌梗死后大鼠心肌组织中的表达及活性变化，以及对相关炎性细胞因子[白细胞介素（IL）-6、IL-10、肿瘤坏死因子-α（TNF-α）]和转录因子（NF—κB、AP-1）表达的影响。方法：结扎冠状动脉左前降支（LAD）近端建立急性心肌梗死（AMI）模型，随机分为AMI组、梗死低剂量PARP抑制剂3-氨基苯甲酰胺（3AB）干预（3AB30）组、梗死高剂量干预（3AB100）组和假手术组。3AB30组和3AB100组分别在腹腔注射3-AB30mg／kg和100mg／kg，AMI组和假手术组给予同等体积0．9％氯化钠溶液腹腔注射。测定各组大鼠术后第1、3、7天心脏功能．非梗死区PARP1的蛋白表达及活性与IL-6、IL-10、TNF-α的表达和转录因子NF-κB和AP-1的活性。结果：心肌梗死后非缺血区PARP1表达在第1天即明显增加，至第7天仍高于假手术组，3AB在非梗死区不仅可以显著抑制TNF-α、IL-6以及PARP1的蛋白表达量和PARP活性，也能够降低NF-κB和AP-1在非梗死区的DNA结合能力。结论：PARPl抑制剂能够明显抑制PARP活性和PARP1表达，在AMI早期通过抑制NF—κB和AP-1活性及炎性因子TNF-α和IL-6表达，能改善心脏功能，减轻心肌损害。

英文摘要：

Objective： To study the protein expression and activation of poly （ADP · ribose） polymerase-1 （PARP1） in noninfarcted myocardium of rats after acute myocardial infarction（AMI）, the protein expression of associated inflammatory cytokines in myocardium and the effect of PARP1 inhibitor 3-AB on heart function after AMI. Method：The AMI models of rats were constructed by LAD ligation. The rats were divided into 5 groups：① AMI group; ②low-dose 3-aminobenzene group ; ③high-dose 3-aminobenzene group; ④ sham group . Cardiac function were determined by the echocardiography at day 1,3,7. The protein expression of PARP1, IL-1β, IL-6, IL-10, and TNF-α in non-infarction regions was measured by immunohistochemical staining . PARP1 activity was determined by Universal Colorimetric PARP Assay Kit with Histone Coated Strip Wells. And the DNA binding activity of NF-κB and AP-1 was detected by EMSA. Result：After AMI the activity of PARP1 significant increased from day 1 till to day 7 in noninfarcted zone. 3AB inhibited both the expression and the enzyme activity of PARP, decreased the expression of IL-6, IL-10, and TNF-α, and the DNA binding activity of NF-κB and AP-1. Conclusion..The PARP1 inhibitor could obviously suppresses the PARP enzyme activity and the PARP1 expression, improve the heart function possibly through inhibiting NF-κB and AP-1 DNA binding activities and the expression of inflammatory factor IL-6, TNF-α.