cerulein


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ce·ru·le·in

(se-rū'lē-in),
A decapeptide with hypotensive activity; stimulates smooth muscle and increases digestive secretions; its structure is similar to cholecystokinin and the gastrins, but much more potent as a stimulant to gallbladder contraction; also stimulates release of insulin. It inhibits fatty acid biosynthesis.
[fr. Cephalosporium caerulea, from which isolated]

ce·ru·le·in

(sĕ-rū'lē-in)
A decapeptide with hypotensive activity, which stimulates smooth muscle and increases digestive secretions. It is similar in structure to cholecystokinin and the gastrins, but much more potent as a stimulant to gallbladder contraction; also stimulates release of insulin.
[fr. Cephalosporium caerulea, from which it is isolated]
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References in periodicals archive ?
In this pancreatitis modelconstructed using cerulein and glycodeoxycholic acid,elevated pancreatic enzymes, edema of pancreatic tissue, and acinar cell necrosis were observed.
established a new model of acute pancreatitis induced by simultaneous and repeated administration of low doses of cerulein (20 [micro]g/kg) and FK156, an activator of NOD1 that mimics the effect of gut bacteria that have breached the mucosal barrier.
Here they found that simultaneous activation of NOD1 and cerulein stimulation of the CCKR led to robust production of C-C motif chemokine ligand 2 (CCL2) by pancreatic acinar cells and that mice deficient in C-C chemokine receptor type 2 (CCR2) did not develop pancreatitis.
took advantage of the low dose cerulein-NOD1 ligand model of experimental acute pancreatitis described above to analyze the separate and synergistic acinar cell signaling induced by simultaneous NOD1 ligand and low dose cerulein stimulation characterizing the induction of pancreatitis.
A second set of insights derived from the low dose cerulein-NOD1 ligand pancreatitis model was that synergistic stimulation by NOD1 ligand and cerulein is also necessary for the optimal generation of Stat3, a signaling component necessary for the upregulation of CCL2 expression, the critically important chemokine necessary for the pancreatic influx of inflammatory macrophages.
Taken together, the model of experimental acute pancreatitis induced by low dose cerulein and NOD1 ligand provides a rich trove of new insights into the immuno-pathogenesis of pancreatitis that is likely to apply to human pancreatitis.
In this chronic model, mice were again administered repeated doses of NOD1 ligand and low doses of cerulein, but in this case this regimen was maintained for a longer period of time.
After treatment with cerulein in the absence or the presence of SFN, pancreatic acinar cells were incubated with fluorescence dye DCFH-DA (Sigma-Aldrich, St.
3 days before AP induction by cerulein hyperstimulation.
Induction of AP with cerulein that resulted in elevation of MDA and pancreatic MDA in mice treated with SFN was reduced as compared with that in cerulein only-treated mice (Figure 2(a)).
As shown in Figure 4(e), SFN administration attenuated enhanced p65 expression as well as its nuclear translocation induced by cerulein.
Cerulein stimulated the expression of NLRP3, casp-1-p20, and cleaved IL-1[beta] in pancreatic acinar cells.