Ghrelin Inhibits the Development of Acute Pancreatitis and Nuclear Factor κB Activation in Pancreas and Liver

Objectives: To investigate the influence of ghrelin on the development of severe acute pancreatitis (SAP) and the expression of nuclear factor kappa B (NF-kappa B) p65 in the pancreas and liver. Methods: Severe acute pancreatitis was induced in rat by sodium taurocholate injection in the pancreaticobiliary duct. Ghrelin was administrated twice at the dose 10 or 20 nmol/kg per injection, respectively. Then, serum amylase activity; serum tumor necrosis factor alpha, interleukin 1 beta, and interleukin 6 concentrations; and morphological signs of pancreatitis and hepatic damage were measured. Meanwhile, determination of pancreatic and hepatic NF-kappa B p65 expression was performed by Western blotting and immunohistochemistry. Results: The serumal parameters increased, and morphological damages were observed in the pancreas and liver in SAP rats. Nuclear factor kappa B p65 expression was significantly higher in the pancreas and liver than sham-operated rats (P < 0.05). Treatment with ghrelin attenuated the morphological damages, and reduced the serumal parameters. Nuclear factor kappa B p65 expression was also significantly reduced by ghrelin (P G 0.05), both in the pancreas and liver. Conclusions: Ghrelin inhibits the development of acute pancreatitis induced by sodium taurocholate. It exerts the therapeutic effects through inhibiting NF-kappa B expression, thereby blocks the inflammatory signal transduction pathway and reduces the release of inflammatory media and cytokines.