Acute pancreatitis was induced in rats in groups 3 and 4 with the infusion of glycodeoxycholic acidinto the biliopancreatic canal and infusion of
cerulein parenterally.
(99-101) Mice deficient in T7 trypsinogen exhibit a marked reduction in activation of trypsinogen but nevertheless exhibit comparable levels of acute and chronic experimental pancreatitis induced by repeated injections of
cerulein, a cholecystokinin receptor (CCKR) agonist as observed in wild type mice.
Xu and colleagues (2015) reported using this model in mice exposed to alcohol and given injections of
cerulein. The mice developed fibrosis and had an increased level of cancerous lesions.
Oxidative stress and inflammatory signaling in
cerulein pancreatitis.
Cerulein-treated mice were composed of mice intraperitoneally injected with
cerulein (Sigma, St Louis, Mo), a cholecystokinin analogue, 7 times on day 0 (dosage, 50 mg/g every hour) to make an acute pancreatitis model.
These scientists developed an in vitro experimental model that allowed them to evaluate how changes in the membrane fatty acid composition in vivo -caused by a change in the type of fat ingested- affect the ability of cells to respond to induced oxidative-inflammatory damage with
cerulein (acute pancreatitis).
Similarly, cftr(-/-) mice showed constitutive expression of proinflammatory cytokines and developed more severe pancreatitis episodes after
cerulein stimulation (22).
Miura et al., "Xanthine oxidase-mediated in response to
cerulein in intracellular oxidative stress rat pancreatic acinar cells," Pancreas, vol.