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  • Title: [The role of lipopolysacchride-binding protein in the pathogenesis of animal model of acute necrotizing pancreatitis].
    Author: Wang XP, Wu LY, Wu K, Zhang RL, Dong YW.
    Journal: Zhonghua Yi Xue Za Zhi; 2003 Sep 25; 83(18):1619-23. PubMed ID: 14642122.
    Abstract:
    OBJECTIVE: To explore the pathogenic role of lipopolysacchride-binding protein (LBP) in the pathogenesis of acute necrotizing pancreatitis (ANP) by applying anti-LBP antibody to the animal model of ANP in mice. METHODS: Sixty BALB/c mice were randomly divided into four groups, including ANP group (n = 18), ANP treated with anti-LBP antibody group (n = 18), anti-LBP antibody group (n = 18) and normal control (n = 6). ANP model was induced by seven times administration of cerulein (50 micro g/kg.body weight), challenged by lipopolysaccharide (LPS) (5 mg/kg) intravenous injection. Treatment with anti-LBP antibody was started 15 minutes before LPS injection in ANP treated with anti-LBP antibody group. Anti-LBP antibody group only received intravenous injection of anti-LBP antibody, normal saline was administrated intraperitoneally instead of cerulein and LPS. At 9 h, 12 h and 24 h after the first injection of cerulein (or saline), the serum levels of amylase and lactate dehydrogenase (LDH) were measured. The severity of pancreatitis was evaluated by histological scoring system. Intrapancreatic TNF-alpha, IL-1beta, ICAM-1 and E-selectin mRNA expressions were studied by semi-quantitative RT-PCR. The activation of nuclear factor-kappaB (NF-kappaB) in the pancreas was investigated by the methods of immunohistochemistry and Western blot. The activity of PMN myeloperoxidase (MPO) was determined by zymohistochemistry. RESULTS: Compared with the ANP group, a marked elevation of serum amylase was observed 9 h and 12 h after cerulein administration and a marked elevation of serum LDH was observed 24 h after cerulein administration in the ANP treated with anti-LBP antibody group. Histologically, treatment with anti-LBP group increased the severity of pancreatic injury including edema at 9 h and 12 h after, and inflammatory cell infiltration and necrosis 24 h after. Intrapancreatic TNF-alpha, IL-1beta, ICAM-1 and E-selectin mRNA levels were increased. The activity of MPO was increased significantly 12 h and 24 h after in the anti-LBP antibody group. Immunohistochemistry and Western blotting showed up-regulation of NF-kappaB. However, there was no significant difference in serum parameters and pathologic scoring results between LBP antibody group and normal control. CONCLUSION: LBP plays a protective role in the pathogenesis of ANP, and this action may be mediated by inhibiting of NF-kappaB activation and down-regulation of proinflammatory mediators.
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