Please use this identifier to cite or link to this item: http://hdl.handle.net/10201/74933

Title: Histopathology and pathogenesis of caerulein-, duct ligation-, and arginine-induced acute pancreatitis in Sprague-Dawley rats and C57BL6 Mice
Issue Date: 2014
Publisher: F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología
Citation: Histology and Histopathology, vol. 29, nº 9, (2014)
ISSN: 1699-5848
0213-3911
Related subjects: CDU::5 - Ciencias puras y naturales::57 - Biología::576 - Biología celular y subcelular. Citología
Keywords: Acute pancreatitis
Arginine
Caerulein
Ductal ligation
Abstract: Three classical rodent models of acute pancreatitis were created in an effort to identify potential pre-clinical models of drug-induced pancreatitis (DIP) and candidate non-invasive biomarkers for improved detection of DIP. Study objectives included designing a lexicon to minimize bias by capturing normal variation and spontaneous and injury-induced changes while maintaining the ability to statistically differentiate degrees of change, defining morphologic anchors for novel pancreatic injury biomarkers, and improving understanding of mechanisms responsible for pancreatitis. Models were created in male SpragueDawley rats and C57BL6 mice through: 1) administration of the cholecystokinin analog, caerulein; 2) administration of arginine; 3) surgical ligation of the pancreatic duct. Nine morphologically detectable processes were used in the lexicon; acinar cell hypertrophy; acinar cell autophagy; acinar cell apoptosis; acinar cell necrosis; vascular injury; interstitial edema, inflammation and hemorrhage; fat necrosis; ductal changes; acinar cell atrophy. Criteria were defined for scoring levels (0= absent, 1= mild, 2= moderate, 3= severe) for each lexicon component. Consistent with previous studies, histopathology scores were significantly greater in rats compared to mice at baseline and after treatment. The histopathology scores in caerulein and ligation-treated rats and mice were significantly greater than those of arginine-treated rats and mice. The present study supports a multifaceted pathogenesis for acute pancreatitis in which intra-acinar trypsinogen activation, damage to acinar cells, fat cells, and vascular cells as well as activation/degranulation of mast cells and activated macrophages all contribute to the initiation and/or progression of acute inflammation of the exocrine pancreas.
Primary author: Zhang, Jun
Rouse, Rodney L.
URI: http://hdl.handle.net/10201/74933
Document type: info:eu-repo/semantics/article
Number of pages / Extensions: 18
Rights: info:eu-repo/semantics/openAccess
Attribution-NonCommercial-NoDerivatives 4.0 International
Appears in Collections:Vol.29, nº 9 (2014)

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