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 ?
Subsequently, cerulein (Sigma & Aldrich Chemie, GmbH, C-9026) was infused for 6 h, 5 [micro]g/kg per hour, with the infusion pump.
Group 4 (ANP[H.sub.2]S, n=13): Like group 3, after acute pancreatitis was formed, 8 mL/kg/h serum physiologic and 5[micro]g/kg cerulein was infused; 8 mL/kg Ringer's lactate was infused for the remaining 18 h.
In initial studies designed to clarify the immune responses against intestinal microflora that might be playing a role in acute pancreatitis Watanabe and his colleagues subjected mice deficient in various innate immune receptors to experimental pancreatitis induced by repeated administration of relatively high doses of cerulein (50 [micro]g/kg), the latter an agent that causes pancreatitis via excessive stimulation of the CCKR.
To further define the role of NOD1 in the development of acute pancreatitis, Watanabe et al., 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.
One of the most commonly used agents for generating the experimental pancreatitis model is cerulein, an analogue of cholecystokinin.
Kim, "Oxidative stress and inflammatory signaling in cerulein pancreatitis," World Journal of Gastroenterology, vol.
Furthermore, in NLRP3 knockout (Nlrp3-/-) mice, cerulein significantly provoked less pancreatic edema, leukocyte infiltration, and acinar cell apoptosis compared to wild-type mice [39], which indicates the importance of the NLRP3 inflammasome in SAP pathogenies.
BALB/c mice received 8 hourly intraperitoneal (i.p.) injections of 0.9% wt/vol saline or saline containing 50 [micro]g/kg body wt of cerulein (Sigma-Aldrich, St.
Numerous studies have demonstrated an early and significant activation of pancreatic NF-[kappa]B when acute experimental pancreatitis is induced in rats or mice using agents such as cerulein, taurocholate, and bile-pancreatic duct ligation [9, 11-13].
Acute pancreatitis can be induced in rats by injection of cerulein, a secretagogue agent.
Experimental AP model was induced by hourly intraperitoneal injections of cerulein (50 [micro]g/kg) to mice for 6 hours.