目的 研究核因子 -κB(NF-κB)活化对大鼠急性坏死性胰腺炎 (ANP)肺损伤中一氧化氮 (NO)的作用。 方法 逆行性胰胆管注射5 %牛磺胆酸钠ANP模型 ,随机分成3组(每组10只) ,对照组 ,ANP组 ,NF-κB抑制剂二硫代氨基甲酸吡咯烷 (PDTC)组。观察模型建立后12h,血清淀粉酶、动脉血氧分压(PaO2)、NO的变化 ,胰腺、肺组织病理变化 ;诱导型一氧化氮合酶(iNOS)及NF-κBp65mRNA在肺组织的表达。结果 PDTC组与ANP组比较 ,血清淀粉酶明显下降 ,由 (8231.20±848.70)U/L降至 (4205.20±1611.49)U/L;NO明显下降 ,由 (178.24±12.00)umol/L降至 (71.00±7.03)umol/L ;胰腺、肺组织损伤减轻 ,iNOS及NF -κBp65mRNA表达下降。结论 抑制NF -κB活化可降低ANP大鼠NO的产生 ,减轻ANP大鼠胰腺炎肺损伤程度 Objective To investigate the effect of nuclear factor-κB (NF-κB) activation on nitric oxide (NO) in lung injury induced by acute necrotizing pancreatitis (ANP) in rats. Methods The retrograde cholangiopancreatography was injected with 5% sodium taurocholate (ANP) and divided into 3 groups (n = 10), control group, ANP group and pyrrolidine dithiocarbamate (PDTC) group. The changes of serum amylase, PaO2 and NO, the pathological changes of pancreas and lung tissue, the expressions of iNOS and NF-κBp65mRNA in the lung tissue were observed 12h after establishment of model. Results Compared with ANP group, serum amylase in PDTC group was significantly decreased from (8231.20 ± 848.70) U / L to (4205.20 ± 1611.49) U / L; NO was significantly decreased from 178.24 ± 12.00 umol / L to 71.00 ± 7.03) umol / L. The damage of pancreas and lung tissue was alleviated and the expression of iNOS and NF-κBp65 mRNA decreased. Conclusion Inhibition of NF-κB activation can reduce NO production in ANP rats and alleviate the degree of lung injury in pancreatitis of ANP rats