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目的 探讨校因子-κB（nuclear factor-kappa B,NF-κB）在重症急性胰腺炎（SAP）肺损伤发病机制中的作用。方法 66只雌性Wistar大鼠随机分为正常组、SAP组、PDTC（二硫代氨基甲酸吡咯烷）预处理组三组。SAP模型采用5％的牛磺胆酸钠1ml/kg胰胆管内逆行注射方法建立。PDTC预处理组在建立SAP模型前1h腹腔内注射PDTC 100ml/kg。后两组分别在3、6、12h三个时相点将动物处死后（各10只）,留取肺组织。应用SP免疫组化方法检测SAP肺组织NF-κB表达情况,运用RT-PCR的方法检测肺组织TNFα、IL-6、ICAM-1mRNA的表达,并测定肺组织湿/干比值作为肺损伤的指标。结果 SAP组肺组织湿/干比值除3h与正常组相比无差异外,其余各组与正常对照组之间有显著性差异（P<0.05）,肺组织内可见NF-κB活化的中性粒细胞浸润,且肺组织TNFα、IL-6、ICAM-1mRNA表达增加。PDTC预处理组肺组织湿/干比值明显降低,NF-κB活化的中性粒细胞明显减少,TNFα、IL-6、ICAM-1 mRNA表达水平显著降低。结论 SAP时存在肺损伤,肺组织NF-κB活化并通过促进TNFα、IL-6、ICAM-1mRNA的表达而参与肺损伤。
Objective To investigate the role of nuclear factor-kappa B (NF-κB) in the pathogenesis of lung injury in severe acute pancreatitis (SAP). Methods Sixty-six female Wistar rats were randomly divided into three groups: normal group, SAP group and PDTC (pyrrolidine dithiocarbamate) pretreatment group. SAP model using 5% sodium taurocholate 1ml / kg retrograde pancreatic duct injections established. The PDTC pretreatment group was intraperitoneally injected with PDTC 100 ml / kg 1 hour prior to SAP model establishment. After the two groups were at 3,6,12 h three time points after the animals were sacrificed (each 10), to collect lung tissue. The expression of NF-κB in SAP lung tissue was detected by SP immunohistochemistry. The expression of TNFα, IL-6 and ICAM-1 mRNA in lung tissue was detected by RT-PCR. The wet / dry ratio of lung tissue was determined as the index of lung injury . Results The wet / dry ratio of lung tissue in SAP group was significantly higher than that in normal group except 3h (P <0.05), and the positive rate of NF-κB activation Granulocyte infiltration, and lung tissue TNFα, IL-6, ICAM-1mRNA expression increased. The wet / dry ratio of lung tissue in PDTC preconditioning group was significantly decreased, the neutrophil activated by NF-κB was significantly decreased, and the expression of TNFα, IL-6 and ICAM-1 mRNA was significantly decreased. Conclusions There is lung injury in SAP and activation of NF-κB in lung tissue, which may be involved in lung injury by promoting the expression of TNFα, IL-6 and ICAM-1 mRNA.