Apamin Attenuated Cerulein-Induced Acute Pancreatitis by Inhibition of JNK Pathway in Mice

作者：Bae Gi Sang; Heo Kwang Ho; Park Kyoung Chel; Choi Sun Bok; Jo Il Joo; Seo Seung Hee; Kim Dong Goo; Shin Joon Yeon; Kang Dae Gil; Lee Ho Sub; Song Ho Joon; Shin Byung Cheul; Park Sung Joo^*

来源：Digestive Diseases and Sciences, 2013, 58(10): 2908-2917.

DOI：10.1007/s10620-013-2800-0

• Bee venom
• Apamin
• Acute pancreatitis
• Cerulein
• c-Jun NH2-terminal kinases

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 mu g/kg) every hour for 6 times. In the apamin treatment group, apamin was administered subcutaneously (10, 50, or 100 mu g/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.

• 出版日期2013-10