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 μg/kg) every hour for 6 times. In the apamin treatment group, apamin was administered subcutaneously (10, 50, or 100 μg/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.
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Acknowledgment
This work was supported by a National Research Foundation of Korea [NRF] grant-funded by the Korean government [MEST]; Contract/Grant Number: 2010-0029498.
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Gi-Sang Bae, Kwang-Ho Heo and Kyoung-Chel Park contributed equally to this work.
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Bae, GS., Heo, KH., Park, KC. et al. Apamin Attenuated Cerulein-Induced Acute Pancreatitis by Inhibition of JNK Pathway in Mice. Dig Dis Sci 58, 2908–2917 (2013). https://doi.org/10.1007/s10620-013-2800-0
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DOI: https://doi.org/10.1007/s10620-013-2800-0