A novel animal model of severe pancreatitis in mice and its differences to the rat

Hartwig, Werner; Schimmel, Eik; Hackert, Thilo; Fortunato, Franco; Bergmann, Frank; Baczako, Andrea; Strobel, Oliver; Büchler, Markus W.; Werner, Jens

doi:10.1016/j.surg.2008.04.006

Cited by 12 publications

(8 citation statements)

References 25 publications

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“…The peak of amylase activity in Na-taurocholate-induced hamster appeared at the 24 hours after infusion of the pancreatic duct ( Fig. 2C ), which is also consistent with the pick of activity in mice 11 and rats 12 . Different from the reports on the L-arginine-induced pancreatitis in mice 13 or rats 14 , the plasma amylase level in L-arginine-induced pancreatitis in hamsters reached peak at 12 hours after first injection of high dose (3 g/kg), and there was no significant increase of plasma amylase level in low dose ( Fig.…”

Section: Resultssupporting

confidence: 83%

“…Na-taurocholate-induced model resembles the gallstone-induced pancreatitis in human. Our results showed that a large area of hemorrhage and necrosis occurred mainly in the anterior but not the posterior of hamster pancreas, which is similar to the pathological characters of mouse 11 and rat 12 models. However, the mortality of the model in the hamster is very low unlike mice 11 , and hamsters have no ascitic fluid accumulation unlike rat 12 either.…”

Section: Discussionsupporting

confidence: 78%

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Experimental Models in Syrian Golden Hamster Replicate Human Acute Pancreatitis

Wang

Kayoumu

et al. 2016

Sci Rep

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The hamster has been shown to share a variety of metabolic similarities with humans. To replicate human acute pancreatitis with hamsters, we comparatively studied the efficacy of common methods, such as the peritoneal injections of caerulein, L-arginine, the retrograde infusion of sodium taurocholate, and another novel model with concomitant administration of ethanol and fatty acid. The severity of pancreatitis was evaluated by serum amylase activity, pathological scores, myeloperoxidase activity, and the expression of inflammation factors in pancreas. The results support that the severity of pathological injury is consistent with the pancreatitis induced in mice and rat using the same methods. Specifically, caerulein induced mild edematous pancreatitis accompanied by minimal lung injury, while L-arginine induced extremely severe pancreatic injury including necrosis and neutrophil infiltration. Infusion of Na-taurocholate into the pancreatic duct induced necrotizing pancreatitis in the head of pancreas and lighter inflammation in the distal region. The severity of acute pancreatitis induced by combination of ethanol and fatty acids was between the extent of caerulein and L-arginine induction, with obvious inflammatory cells infiltration. In view of the advantages in lipid metabolism features, hamster models are ideally suited for the studies of pancreatitis associated with altered metabolism in humans.

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Section: Resultssupporting

confidence: 83%

Section: Discussionsupporting

confidence: 78%

Experimental Models in Syrian Golden Hamster Replicate Human Acute Pancreatitis

Wang

Kayoumu

et al. 2016

Sci Rep

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“…Longer durations of ischemia resulted signs of acute distress in recipients, requiring early sacrifice. Murine models of pancreatitis elicit increases in serum amylase and LDH (11). The present model similarly demonstrated chemical pancreatitis that peaked 6 hours following reperfusion and normalized by 120 hours.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of IL-1β, IL-6, and CCL-2 by a Novel Mouse Model of Pancreatic Ischemia-Reperfusion Injury

et al. 2013

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Little is known about the immunologic events surrounding pancreatic ischemia-reperfusion injury (IRI) due to a lack of established experimental models. The purpose of the current study was to develop a mouse model for pancreatic IRI to serve as a basis for immunologic characterization of pancreatic organ damage at transplantation. Methods Reversible ischemia was surgically induced by vascular isolation of the distal pancreas for 0, 10, 20, or 30 minutes. Mice receiving laparotomy without clamping served as sham-operated controls. Following reperfusion, mice were serially assayed for biochemical and histologic evidence of inflammation, proinflammatory cytokine and chemokine production, and inflammatory gene up-regulation. Results Following induction of pancreatic IRI, serum amylase and LDH peaked at 6 hours and returned to baseline by 120 hours following injury in all groups. Mice undergoing 30 minutes of IRI demonstrated greatest biochemical evidence of inflammation. Histologic scoring similarly demonstrated marked inflammation in mice subjected to 30 minutes IRI compared to controls. Serum cytokine/chemokine analysis demonstrated significant up-regulation of G-CSF, IFN-γ, TNF-α, IL-2, IL-1β, IL-6, CCL-2, CCL-5, CXCL-1, and MIP-2. Similar up-regulation of ccl2, il1b, il6, fos, hspa1a, hspd1, and cd14 gene expression was detected by real-time PCR analysis of pancreatic tissue. Conclusions This novel model of distal pancreatic IRI in the mouse demonstrates time-limited pancreatic inflammation and injury by histologic and biochemical indices. Inflammation may be, in part, a result of the immunologic effects of IL-1β, IL-6, and CCL-2. This model provides a method by which immunologic mechanisms of pancreatic IRI can be elucidated.

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“…Another fragment of the pancreas was snap-frozen in liquid nitrogen for the measurement of trypsin activity. Trypsin activity was analysed using pancreatic tissue extract and the fluorochromic substrate Gln-Ala-Arg-AMC (where AMC is 7-amino-4-methylcoumarin) as previously described 31 32. Serum amylase and lipase were measured using the ADVIA-2400 chemistry system (BayerHealthCare, Leverkusen, Germany).…”

Section: Methodsmentioning

confidence: 99%