Journal
PANCREAS
Volume 36, Issue 2, Pages E22-E29Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MPA.0b013e31815a396b
Keywords
bee venom; cholecystokinin octapeptide; acute pancreatitis; proinflammatory cytokines; NF-kappa B binding activity
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Objectives: Bee venom (BV) has frequently been used as a remedy for inflammatory diseases. The aim of this study was to investigate the effect of BV on cholecystokinin octapeptide (CCK-8)-induced acute pancreatitis (AP) in rats. Methods: The BV pretreatment group: 0.25 mg/kg BV was administered subcutaneously, followed by 75 Kg/kg CCK-8 subcutaneously 3 times after 1, 3, and 5 hours. This whole procedure was repeated for 5 days. Control group: CCK- 8 subcutaneously 3 times after 1, 3, and 5 hours for 5 days. The BV posttreatment group: CCK8 subcutaneously 3 times at an interval of 2 hours for 3 days, and then 0.25 mg/kg of BV was administered subcutaneously. Control group: CCK- 8 subcutaneously 3 times at an interval of 2 hours for 3 days. Results: The BV pretreatment and posttreatment ameliorated many of the examined laboratory parameters (the pancreatic weight [PW]/body weight [BW] ratio, the serum amylase and lipase activity) and reduced histological damages in pancreas. Furthermore, BV pretreatment reduced the production of tumor necrosis factor-alpha, interleukin 1, and interleukin 6 and also decreased pancreatic nuclear factor-kappa B binding activity compared with saline-treated group in the AP model. The BV also increased heat shock protein 60 (HSP60) and heat shock protein 72 (HSP72) compared with the saline-treated group in the AP model. Conclusions: These findings suggest that the anti-inflammatory effect of BV in CCK-8-induced AP seems to be mediated by inhibiting nuclear factor-kappa B binding activity, and that BV may have a protective effect against AP.
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