| Obstructive jaundice is a common pathosis in clinic. Caused by either benign or malignant disease, Obstructive jaundice is associated with a high rate of postoperative complications. Infection, bleeding, impaired wound healing, renal failure, liver failure, sepsis are common. Study in these years indicates that impaired immune function probably contributes to most of these complications. Inflammatory induced by endotoxin, overexpression of inflammatory media and liver injury caused by inflammatory media may result in impaired immune function. Nuclear factor-κB (NF-κB), ubiquitously expressed in most eukaryon cell types, is a transcription factor that plays a critical role in both innate and adaptive immune responses by regulating the gene expression of many cellular media. The activated NF-κB can bind to the acception on the nuclear membrane and then translocate into the nucleus, where it combine to special DNA and regulates the expression of hundreds of genes that are important in immune and inflammatory responses. These genes include genes for cytokines (for example turner necrosis factor-α, interleukin-1), adhesion molecules, members of the major histocompatibility complex, proteins involved in antigen presentation. Our study is to investigate the regulation of NF-κB on expression of inflammatory media in the liver, its role in liver injury in rats with obstructive jaundice and the protective effect of pyrrolidine dithiocarbamate (PDTC) in the live injury caused by obstructive jaundice.We set up a model of obstructive jaundice in rats. Fifty four Sprague-Dawley rats were randomized into three groups: Sham group, common bile duet ligation group (CBDL group) and group of PDTC treated (PDTC group). The rats in sham group were only exposed the common bile duct. Common bile ducts in rats of CBDL group were ligated and sectioned. The rats in PDTC group were treated by PDTC (intraperitoneal injection) before and after operation. Total bilirubin (TB), serum alanine transminase (ALT), hepatic NF-κB activities and the expression of turner necrosis factor-α(TNF-α) mRNA, interleukin-6 (IL-6) mRNA, intracellular adhesion molecule-1 (ICAM-1) mRNA were examined in the three group at the time spot of 4d, 7d, 14d after operation. Using SPSS 10.0, data are expressed as means±S.E.M. Statistical analysis was performed using one-way analysis of variance followed by Student-Newman-Keuls multiple comparison. Coefficients of correlation were analyzed between NF-κB and TNF-αmRNA, IL-6mRNA, ICAM-1 mRNA. A P value of less than 0.05 was considered statistically significant.4, 7 or 14 days after operation, the hepatic injury appeared with the elevation of serum ALT, total bilirubin (TB). The level of hepatic NF-κB P65 obviously elevated with the prolongation of obstructive jaundice. The transcription of TNF-α, IL-6 and ICAM-lsignificantly increased on 4, 7 and 14 days after operation. PDTC treatment significantly decreased the content of NF-κB P65 in the liver in concurrence with the expression of ICAM-1. The level of serum ALT and hepatic expression of TNF-αmRNA were decreased 4 or 7d after administration of PDTC.Hepatic NF-κB is activated in rats with obstructive jaundice. The activation of hepatic NF-κB is associated with the liver injury by regulating expression of proinflammatory mediators. PDTC protect the liver from early inflammatory injury in obstructive jaundice.
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