Apamin Attenuated Cerulein-Induced Acute Pancreatitis by Inhibition
of JNK Pathway in Mice
Dig Dis Sci, 2013 Aug 6
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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