November 12, 2014
Notes: Bachmann, Kai
Izbicki, Jakob R
Randomized Controlled Trial
Ann Surg. 2013 Nov;258(5):815-20; discussion 820-1. doi: 10.1097/SLA.0b013e3182a655a8.
Author Address: From the Department of General Surgery, University Hospital Hamburg Eppendorf, Hamburg, Germany.
Reference Type: Journal Article
Record Number: 5046Author: Bae, G. S., Heo, K. H., Park, K. C., Choi, S. B., Jo, I. J., Seo, S. H., Kim, D. G., Shin, J. Y., Kang, D. G., Lee, H. S., Song, H. J., Shin, B. C. and Park, S. J.
Title: Apamin attenuated cerulein-induced acute pancreatitis by inhibition of JNK pathway in mice
Journal: Dig Dis Sci
Short Title: Apamin attenuated cerulein-induced acute pancreatitis by inhibition of JNK pathway in mice
Alternate Journal: Digestive diseases and sciences
ISSN: 1573-2568 (Electronic)
Accession Number: 23918150
Keywords: Acute Disease
Apamin/administration & dosage/*pharmacology/*therapeutic use
Ceruletide/administration & dosage/*adverse effects
Cholecystokinin/analogs & derivatives
Disease Models, Animal
MAP Kinase Signaling System/*drug effects/physiology
Mice, Inbred C57BL
Mitogen-Activated Protein Kinase Kinases/metabolism
Pancreatitis/*chemically induced/*prevention & control
Abstract: BACKGROUND/AIM: We have previously reported that bee venom (BV) has a protective role against acute pancreatitis (AP). However, the effects of apamin, the major compound of BV, on AP have not been determined. The aim of this study was to evaluate the effects of apamin on cerulein-induced AP. METHODS: AP was induced via intraperitoneal injection of supramaximal concentrations of the stable cholecystokinin analogue cerulein (50 mug/kg) every hour for 6 times. In the apamin treatment group, apamin was administered subcutaneously (10, 50, or 100 mug/kg) at both 18 and 1 h before the first cerulein injection. The mice were sacrificed at 6 h after the final cerulein injection. Blood samples were obtained to determine serum amylase and lipase levels, as well as cytokine production. The pancreas and lung were rapidly removed for morphologic and histological examination, myeloperoxidase (MPO) assay, and real-time reverse transcription-polymerase chain reaction. Furthermore, we isolated the pancreatic acinar cells to specify the role of apamin in AP. RESULTS: Pre-treatment with apamin inhibited histological damage, pancreatic weight/body weight ratio, serum level of amylase and lipase, MPO activity, and cytokine production. In addition, apamin treatment significantly inhibited cerulein-induced pancreatic acinar cell death. Furthermore, apamin treatment inhibited the cerulein-induced activation of c-Jun NH2-terminal kinases (JNK). CONCLUSIONS: These results could suggest that apamin could protect against AP by inhibition of JNK activation.