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目的:探讨PARP-1[poly （ADP-ribose） polymerase-1，聚腺苷酸二磷酸核糖转移酶-1]在重症急性胰腺炎（severe acute pancreatitis, SAP）大鼠肠黏膜屏障损伤中的作用机制。方法:20只Wistar大鼠按随机数字表法分为CON组（对照组）、SAP组、3-AB组（即PARP-1抑制剂组）、3-AB-CON组，每组各5只。腹腔注射雨蛙素及脂多糖制作SAP大鼠模型，CON组仅注射等体积生理盐水，3-AB组于建模前0.5 h注射3-AB溶液30 mg/kg，3-AB-CON组腹腔注射3-AB溶液30 mg/kg 0.5 h后处理同CON组。各组大鼠建模后12 h处死，观察各组腹腔内大体改变，取心脏血、胰腺和肠组织，光镜下观察胰腺组织及肠组织病理形态学改变，采用酶联免疫吸附试验（ELISA）检测血清白细胞介素-6（IL-6）含量，使用全自动生化仪检测血清淀粉酶含量，采用蛋白免疫印迹试验（Western Blot）测定肠组织PARP-1、胞核核转录因子-κB（NF-κB）的蛋白表达，采用免疫组化试验测定肠黏膜Occludin蛋白表达。计量资料多组间比较采用单因素方差分析，方差不齐时则用秩转换的非参数检验，以n P<0.05为差异有统计学意义。n 结果:与CON组比较，SAP组大鼠腹腔明显腹水，胰腺病理明显出血坏死，肠组织绒毛结构紊乱，淀粉酶、IL-6水平升高，肠组织PARP-1、NF-κB蛋白表达明显增多，肠黏膜Occludin蛋白表达减少，说明PARP-1可诱导NF-κB活化和炎症损伤，导致胰腺及肠损伤。3-AB-CON组与CON组各指标比较差异无统计学意义。与SAP组比较，3-AB组胰腺及肠组织损伤明显减轻，淀粉酶、IL-6水平明显降低[淀粉酶（U/L）（1 879.25±736.66） n vs （5 569.33±1 993.48），IL-6（pg/mL）（77.98±20.65） n vs （209.14±79.08），均n P<0.05],肠组织PARP-1、胞核NF-κB蛋白表达减少[PARP-1（灰度值）（1.44±0.09） n vs （1.49±0.13），NF-κB（灰度值）（0.63±0.09） n vs （0.96±0.08）,均n P<0.05]，肠黏膜Occludin蛋白表达增多[评分（6.7±1.5） n vs （3.2±1.1），n P<0.05]。n 结论:抑制PARP-1表达对SAP肠黏膜屏障损伤有保护作用，其作用机制可能是通过抑制NF-κB信号通路、增加肠黏膜Occludin蛋白表达有关。“,”Objective:To investigate the effects of poly (ADP-ribose) polymerase-1(PARP-1) in intestinal mucosal barrier injury in rat model with severe acute pancreatitis (SAP).Methods:Twenty healthy male Wistar rats were divided into four groups (n n=5 each group) using a random table method: control, SAP, 3-aminobenzamide (3-AB), and 3-AB control groups. The SAP model was induced by intraperitoneal injection of cerulean with lipopolysaccharide. At 30 min, the rats were treated with the PARP-1 inhibitor, 3-AB, or normal saline,separately. After 12 h, all rats were sacrificed to harvest pancreas tissues, intestines tissues, and blood from the hearts for index detection. Serum amylase (AMY) and interleukin (IL)-6 levels were measured using an automatic biochemical instrument and enzyme-linked immunosorbent assay (ELISA), respectively.The protein expression of PARP-1 and nuclear factor (NF-κB) were measured using Western blot and that of occludin was measured using an immunohistochemical test. One-way analysis of variance was used for comparison of multiple groups of variables. Non-parametric tests of rank conversion were used when variances were not uniform. An P <0.05 was considered statistically significant.n Results:Compared to the control group, the following indexes in the SAP group were significantly increased: ascites (with serious hemorrhage and necrosis in the pancreas and disordered intestinal villi),serum AMY and IL-6 levels, and the expression of PARP-1 and NF-κB. However, Occludin expression was significantly decreased. There was no significant difference between 3-AB group and 3-AB control group. Compared to the SAP group, the severity of SAP and pancreatitis-associated intestinal injury was significantly attenuated with the administration of 3-AB. Serum AMY and IL-6 levels were significantly decreased (serum AMY: 1 879.25 ± 736.6 U/Ln vs 5 569.33 ± 1993.48 U/L; IL-6: 77.98 ± 20.65 pg/mL n vs 209.14 ± 79.08 pg/mL, both n P<0.05), but the expression of PARP-1 and NF-κB were significantly increased (PARP-1: 1.44 ± 0.09n vs 1.49 ± 0.13; NF-κB: 0.63 ± 0.09n vs 0.96±0.08, both n P<0.05). Similarly, Occludin expression was significantly decreased (6.7±1.5 n vs 3.2±1.1, n P<0.05).n Conclusions:Inhibition of PARP-1 has protective effects on SAP associated intestinal mucosal barrier damage. The mechanism may be related to the inhibition of NF-κB signaling pathway and increase intestinal mucosal Occludin protein expression.