The Role of Nuclear Factor-kappa B in the Pathogenesis of Severe Acute Pancreatitis-Associted Lung Injury

Objective To investigate the role of NF-κB(nuclear factor kappa B,NF-κB) in the pathogenesis of severe acute pancreatitis-associated lung injury. Methods Sixty-six female Wistar rats were divided into normal group, SAP group and PDTC pretreated group. Pancreatitis was induced by intraductal administration of 5% sodium taurocholate. Pyrrolidine dithiocarbamate(PDTC) pretreated SAP rats was given 100 mg/kg PDTC intraperitoneally before pancreatitis was induced. Rats in SAP group, PDTC pretreated group were killed at 3,6,12 hours after induction of the model. NF-κB activity in lung tissue was detected by immunohistochemical methods. The mRNA expression of TNFα. IL-6. ICAM-1 in lung was evaluated by reverse transcription-polymerase chain reaction. We measured the ratio of wet/dry tissue as lung injury index. Results The ratio of wet/dry tissue and the levels of TNFα. IL-6. ICAM-1 mRNA increased significantly in lung tissue in SAP group comparing with normal group. The activity of NF-κB increased significantly in lung tissue from SAP group rats. PDTC decreased the ratio of wet/dry tissue, NF-kB activity in lung tissue(P0.05) and the level of TNFα,IL-6. ICAM-1 mRNA in lung tissue (P0.05). Conclusions There exits lung injury associated with SAP. NF-κB play damage role in severe acute pancreatitis-associated lung injury by promoting TNFα, IL-6, ICAM-1 mRNA expression. The result demonstrates that inhibition of NF-κB activity may be a promising strategy in the treatment of SAP.