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Acute pancreatitis:The stress factor

World Journal of gastroenterology 2014年第19期20卷 5801-5807页

作者： marcelo g binker Laura I Cosen-binker CBRHC Research Center 1053 Ciudad Autónoma de Buenos AiresBuenos Aires 1426Argentina Department of Molecular and Cell Biology Henry M Goldman School of Dental MedicineBoston UniversityBostonMA 02118United States

Acute pancreatitis is an inflammatory disorder of the pancreas that may cause life-threatening *** of pancreatitis vary,with gallstones accounting for the majority of all cases,followed by *** causes of pancreatitis include trauma,ischemia,mechanical obstruction,infections,autoimmune,hereditary,and *** main events occurring in the pancreatic acinar cell that initiate and propagate acute pancreatitis include inhibition of secretion,intracellular activation of proteases,and generation of inflammatory *** cytokines known as chemokines are released from damaged pancreatic cells and attract inflammatory cells,whose systemic action ultimately determined the severity of the ***,severe forms of pancreatitis may result in systemic inflammatory response syndrome and multiorgan dysfunction syndrome,characterized by a progressive physiologic failure of several interdependent organ *** occurs when homeostasis is threatened,and stressors can include physical or mental forces,or combinations of *** on the timing and duration,stress can result in beneficial or harmful *** it is well established that a previous acute-short-term stress decreases the severity of experimentally-induced pancreatitis,the worsening effects of chronic stress on the exocrine pancreas have received relatively little *** review will focus on the influence of both prior acute-short-term and chronic stress in acute pancreatitis.

关键词： Pancreatitis Acute stress Chronic stress Heat shock proteins Tumor necrosis factor alpha

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Chronic stress sensitizes rats to pancreatitis induced by cerulein:Role of TNF-α

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World Journal of gastroenterology 2010年第44期16卷 5565-5581页

作者： marcelo g binker Andres A binker-Cosen Daniel Richards Herbert Y gaisano Rodica H de Cosen Laura I Cosen-binker CBRHC Research Health Center Department of Medicine and Physiology University of Toronto

AIM:To investigate chronic stress as a susceptibility factor for developing pancreatitis,as well as tumor necrosis factor-α (TNF-α) as a putative ***:Rat pancreatic acini were used to analyze the influence of TNF-α on submaximal (50 pmol/L) cholecystokinin (CCK) *** restraint (4 h every day for 21 d) was used to evaluate the effects of submaximal (0.2 μg/kg per hour) cerulein stimulation on chronically stressed ***:In vitro exposure of pancreatic acini toTNF-α disorganized the actin *** was further increased by TNF-α/CCK treatment,which additionally reduced amylase secretion,and increased trypsin and nuclear factor-κB activities in a protein-kinase-C δ and ε-dependent ***-α/CCK also enhanced caspases' activity and lactate dehydrogenase release,induced ATP loss,and augmented the ADP/ATP *** vivo,rats under chronic restraint exhibited elevated serum and pancreatic TNF-α ***,pancreatic,and lung inflammatory parameters,as well as caspases' activity in pancreatic and lung tissue,were substantially enhanced in stressed/cerulein-treated rats,which also experienced tissues' ATP loss and greater ADP/ATP *** examination revealed that stressed/cerulein-treated animals developed abundant pancreatic and lung edema,hemorrhage and leukocyte infiltrate,and pancreatic *** severity was greatly decreased by treating animals with an anti-TNF-αantibody,which diminished all inflammatory parameters,histopathological scores,and apoptotic/necrotic markers in stressed/cerulein-treated ***:In rats,chronic stress increases susceptibility for developing pancreatitis,which involves TNF-α sensitization of pancreatic acinar cells to undergo injury by physiological cerulein stimulation.

关键词： Pancreatitis Stress Tumor necrosis factor-α

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Relaxin prevents the development of severe acute pancreatitis

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World Journal of gastroenterology 2006年第10期12卷 1558-1568页

作者： Laura Iris Cosen-binker marcelo gustavo binker Rodica Cosen gustavo Negri Osvaldo Tiscornia RHC-LICB Medical Research Institute-Buenos Aires Argentina Programa de Estudios Pancreáticos-Hospital de Clinicas Universidad de Buenos AiresArgentina Cátedra de Gastroenterologia y Enzimologia Clinica-Departamento de Bioquimica ClinicaFacultad de Farmacia y BioquimicaUniversidad de Buenos AiresArgentina RHC-LICB Medical Research Institute-Buenos Aires Argentina Programa de Estudios Pancreáticos-Hospital de Clínicas Universidad de Buenos AiresArgentina RHC-LICB Medical Research Institute-Buenos Aires Argentina Cátedra de gastroenterología y Enzimología Clínica-Departamento de Bioquímica Clínica Facultad de Farmacia y Bioquimica Universidad de Buenos AiresArgentina Programa de Estudios Pancreáticos-Hospital de Clínicas Universidad de Buenos Aires Argentina

AIM： TO investigate the severity of acute pancreatitis （AP） is associated to the intensity of leukocyte activation, inflammatory up-regulation and microcirculatory disruption associated to ischernia-reperfusion injury. Hicrovascular integrity and inhibition of pro-inflammatory mediators are key-factors in the evolution of AP. Relaxin is an insulin-like hormone that has been attributed vasorelaxant properties via the nitric oxide pathway while behaving as a glucocorticoid receptor agonist. METHODS： AP was induced by the bilio-pancreatic duct-outlet-exclusion closed-duodenal-loops model. Treatment with relaxin was done at different timepoints. Nitric oxide synthase inhibition by L-NAME and glucocorticoid receptor （gR） blockage by mifepristone was considered. AP severity was assessed by biochemical and histopathological analyses. RESULTS： Treatment with relaxin reduced serum amylase, lipase, C-reactive protein, IL-6, IL-10, hsp72, LDH and 8-isoprostane as well as pancreatic and lung myeloperoxidase. Acinar and fat necrosis, hemorrhage and neutrophil infiltrate were also decreased. ATP depletion and ADP/ATP ratio were reduced while caspases 2-3-8 and 9 activities were increased. L-NAME and mifepristone decreased the efficiency of relaxin. CONCLUSION： Relaxin resulted beneficial in the treatment of AP combining the properties of a gR agonist while preserving the microcirculation and favoring apoptosis over necrosis.

关键词： Acute pancreatitis Relaxin Nitric oxide glucocorticoid receptor Necrosis Apoptosis

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Munc18/SNARE proteins’ regulation of exocytosis in guinea pig duodenal Brunner’s gland acini

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World Journal of gastroenterology 2008年第15期14卷 2314-2322页

作者： Laura I Cosen-binker gerry P Morris Stephen Vanner Herbert Y gaisano Department of Medicine University of Toronto Toronto Ontario M5S 1A8 Canada gastrointestinal Diseases Research Unit Queen's University Kingston Ontario KL7 5G2 Canada

AIM: To examine the molecular mechanism of exocytosis in the Brunner’s gland acinar cell. METHODS: We used a submucosal preparation of guinea pig duodenal Brunner’s gland acini to visualize the dilation of the ductal lumen in response to cholinergic stimulus. We correlated this to electron microscopy to determine the extent of exocytosis of the mucin-filled vesicles. We then examined the behavior of SNARE and interacting Munc18 proteins by confocal microscopy. RESULTS: One and 6 μmol/L carbachol evoked a dose- dependent dilation of Brunner’s gland acini lumen, which correlated to the massive exocytosis of mucin. Munc18c and its cognate SNARE proteins Syntaxin-4 and SNAP-23 were localized to the apical plasma membrane, and upon cholinergic stimulation, Munc18c was displaced into the cytosol leaving Syntaxin-4 and SNAP-23 intact. CONCLUSION: Physiologic cholinergic stimulation induces Munc18c displacement from the Brunner’s gland acinar apical plasma membrane, which enables apical membrane Syntaxin-4 and SNAP-23 to form a SNARE complex with mucin-filled vesicle SNARE proteins to affect exocytosis.

关键词： Apical exocytosis Brunner's gland acini Munc18c Syntaxin-4 Carbachol

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