Relevant bibliographies by topics / Experimental acute pancreatitis ; L-arginine induced acute pancreatitis

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Academic literature on the topic 'Experimental acute pancreatitis ; L-arginine induced acute pancreatitis'

Author: Grafiati
Published: 4 June 2021
Last updated: 4 February 2022

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Journal articles on the topic "Experimental acute pancreatitis ; L-arginine induced acute pancreatitis"

1

Jamdar, S., B. I. Babu, M. Nirmalan, M. Jeziorska, R. F. McMahon, and K. Siriwardena. "ACTIVATED PROTEIN C IN L-ARGININE-INDUCED EXPERIMENTAL ACUTE PANCREATITIS." Pancreas 37, no. 4 (2008): 476. http://dx.doi.org/10.1097/01.mpa.0000335482.92345.52.

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2

Dawra, Rajinder, Rifat Sharif, Phoebe Phillips, Vikas Dudeja, Dhara Dhaulakhandi, and Ashok K. Saluja. "Development of a new mouse model of acute pancreatitis induced by administration of l-arginine." American Journal of Physiology-Gastrointestinal and Liver Physiology 292, no. 4 (2007): G1009—G1018. http://dx.doi.org/10.1152/ajpgi.00167.2006.

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The pathogenesis of acute pancreatitis is not fully understood. Experimental animal models that mimic human disease are essential to better understand the pathophysiology of the disease and to evaluate potential therapeutic agents. Given that the mouse genome is known completely and that a large number of strains with various genetic deletions are available, it is advantageous to have multiple reliable mouse models of acute pancreatitis. Presently, there is only one predominant model of acute pancreatitis in mice, in which hyperstimulatory doses of cholecystokinin or its analog caerulein are administered. Therefore, the aim of this study was to develop another mouse model of acute pancreatitis. In this study, C57BL/6 mice were injected intraperitoneally with l-arginine in two doses of 4 g/kg each, 1 h apart. Serum amylase, myeloperoxidase, and histopathology were examined at varying time points after injection to assess injury to the pancreas and lung. We found that injection of l-arginine was followed by significant increases in plasma amylase and pancreatic myeloperoxidase accompanied by marked histopathological changes. The injury to the pancreas was slow to develop and peaked at 72 h. Subsequent to peak injury, the damaged areas contained collagen fibers as assessed by increased Sirius red staining. In contrast, d-arginine or other amino acids did not cause injury to the pancreas. In addition, acute inflammation in the pancreas was associated with lung injury. Our results indicate that administration of l-arginine to mice results in severe acute pancreatitis. This model should help in elucidating the pathophysiology of pancreatitis.
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3

Chen, Guolin, Feng Xu, Jing Li, and Shiqi Lu. "Depletion of Neutrophils Protects Against L-Arginine-Induced Acute Pancreatitis in Mice." Cellular Physiology and Biochemistry 35, no. 6 (2015): 2111–20. http://dx.doi.org/10.1159/000374017.

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Background/Aims: Acute pancreatitis (AP) is an inflammatory disease characterized by acinar cell damage and inflammation of the pancreas with infiltration of leukocytes, predominantly neutrophils. We investigated whether neutrophil depletion protects against experimental AP induced by L-arginine. Methods: AP was induced in C57BL/6 mice via two intraperitoneal L-arginine (4 g/kg) injections. Mice were pretreated with 250 and 100 µg anti-Gr-1 antibody via intraperitoneal injection at 24 and 4 h, respectively, before L-arginine challenge for neutrophil depletion. At 48 and 72 h after injection, the severity of AP was determined with the aid of biochemical and histological analyses. Amylase and MPO activity was detected using specific assay kits. The plasma cytokines levels were detected using ELISA. Results: Neutrophil depletion resulted in significantly reduced plasma amylase levels in pancreas, myeloperoxidase (MPO) activity in pancreas and lung, reactive oxygen species (ROS) generation and cell apoptosis, and decreased circulating neutrophil, tissue damage as well as expression levels of nuclear factor NF-κB. Conclusion: Neutrophil depletion is capable of reducing tissue damage of pancreas and lung in mice with acute pancreatitis.
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4

Dixit, Ajay, Hassam Cheema, John George, et al. "Extracellular release of ATP promotes systemic inflammation during acute pancreatitis." American Journal of Physiology-Gastrointestinal and Liver Physiology 317, no. 4 (2019): G463—G475. http://dx.doi.org/10.1152/ajpgi.00395.2018.

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In the current study, we explored the role of extracellular ATP (eATP) in promoting systemic inflammation during development of acute pancreatitis (AP). Release of extracellular (e)ATP was evaluated in plasma and bronchoalveolar lavage fluid (BALF) of mice with experimental acute pancreatitis (AP). Prophylactic intervention using apyrase or suramin was used to understand the role and contribution of eATP in pancreatitis-associated systemic injury. AP of varying severity was induced in C57BL/6 mice using 1-day or 2-day caerulein, caerulein + LPS and l-arginine models. eATP was measured in plasma and BALF. Mice were treated with suramin or apyrase in the caerulein and l-arginine models of AP. Plasma cytokines, lung, and pancreatic myeloperoxidase, and morphometric analysis of pancreatic and lung histology, were used to assess the severity of pancreatitis. Plasma eATP and purinergic 2 (P2) receptors in the pancreas and lungs were significantly elevated in the experimental models of AP. Blocking the effect of eATP by suramin led to reduced levels of plasma IL-6 and TNFα as well as reduced lung, and pancreatic injury. Neutralizing eATP with apyrase reduced systemic injury but did not ameliorate local injury. The results of this study support the role of eATP and P2 receptors in promoting systemic inflammation during AP. Modulating purinergic signaling during AP can be an important therapeutic strategy in controlling systemic inflammation and, thus, systemic inflammatory response syndrome during AP. NEW & NOTEWORTHY Released ATP from injured cells promotes systemic inflammation in acute pancreatitis
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5

Santana, Danielle Gomes, Alan Santos Oliveira, Marília Trindade de Santana Souza, et al. "Vaccinium macrocarponAiton Extract Ameliorates Inflammation and Hyperalgesia through Oxidative Stress Inhibition in Experimental Acute Pancreatitis." Evidence-Based Complementary and Alternative Medicine 2018 (2018): 1–13. http://dx.doi.org/10.1155/2018/9646937.

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We evaluated the effect of the hydroethanolic extract of fruits ofVaccinium macrocarpon(HEVm) in a model of acute pancreatitis (AP) in mice. AP was induced by two injections of L-arginine and animals were treated with HEVm (50, 100, and 200 mg/kg, p.o.) or vehicle (saline) every 24 h, starting 1 h after the induction of AP. Phytochemical analysis of the extract and measurement of inflammatory and oxidative stress parameters, as well as abdominal hyperalgesia, were performed. Catechin, epicatechin, rutin, and anthocyanins were identified in HEVm. Treatment with HEVm decreased L-arginine-induced abdominal hyperalgesia (from 48 to 72 h). Also, treatment with HEVm decreased L-arginine-induced pancreatic edema, pancreatic and pulmonary neutrophil infiltration, and levels of tumor necrosis factor-α, interleukin-1β, and interleukin-6, after 72 h of induction. L-arginine-induced hyperamylasemia and hyperlipasemia were also reduced by the treatment with HEVm in comparison to vehicle-treated group. Moreover, lipoperoxidation, carbonyl radicals, nonprotein sulfhydryl groups, and activity of catalase and superoxide dismutase, but not glutathione peroxidase, were restored by the treatment with HEVm. These results show that treatment with HEVm decreased hyperalgesia and pancreatic/extrapancreatic inflammation and oxidative damage in L-arginine-induced AP, making this extract attractive for future approaches designed to treat this condition.
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6

Kubisch, Constanze H., Maria Dolors Sans, Thiruvengadam Arumugam, Stephen A. Ernst, John A. Williams, and Craig D. Logsdon. "Early activation of endoplasmic reticulum stress is associated with arginine-induced acute pancreatitis." American Journal of Physiology-Gastrointestinal and Liver Physiology 291, no. 2 (2006): G238—G245. http://dx.doi.org/10.1152/ajpgi.00471.2005.

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Endoplasmic reticulum (ER) stress mechanisms have been found to play critical roles in a number of diseases states, such as diabetes mellitus and Alzheimer disease, but whether they are involved in acute pancreatitis is unknown. Here we show for the first time that all major ER stress sensing and signaling mechanisms are present in exocrine acini and are activated early in the arginine model of experimental acute pancreatitis. Pancreatitis was induced in rats by intraperitoneal injection of 4.0 g/kg body wt arginine. Pancreatitis severity was assessed by analysis of serum amylase, pancreatic trypsin activity, water content, and histology. ER stress-related molecules PERK, eIF2α, ATF6, XBP-1, BiP, CHOP, and caspase-12 were analyzed. Arginine treatment induced rapid and severe pancreatitis, as indicated by increased serum amylase, pancreatic tissue edema, and acinar cell damage within 4 h. Arginine treatment also caused an early activation of ER stress, as indicated by phosphorylation of PERK and its downstream target eIF2α, ATF6 translocation into the nucleus (within 1 h), and upregulation of BiP (within 4 h). XBP-1 splicing and CHOP expression were observed within 8 h. After 24 h, increased activation of the ER stress-related proapoptotic molecule caspase-12 was observed along with an increase in caspase-3 activity and TdT (terminal deoxynucleotidyl transferase)-mediated dUDP nick-end labeling (TUNEL) staining in exocrine acini. These results indicate that ER stress is an important early acinar cell event that likely contributes to the development of acute pancreatitis in the arginine model.
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7

Li, Yong, Yiyuan Pan, Lin Gao, et al. "Naringenin Protects against Acute Pancreatitis in Two Experimental Models in Mice by NLRP3 and Nrf2/HO-1 Pathways." Mediators of Inflammation 2018 (2018): 1–13. http://dx.doi.org/10.1155/2018/3232491.

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Background. Naringenin (Nar) is a type of flavonoid and has been shown to have anti-inflammatory and antioxidative properties. However, the effects of Nar on acute pancreatitis (AP) have not been well studied. In this study, we aimed to investigate the function of Nar in a mouse model of AP. Methods. Mild acute pancreatitis (MAP) was induced by caerulein (Cae), and severe acute pancreatitis (SAP) was induced by L-arginine in mice. Nar was administered intraperitoneally at doses of 25, 50, or 100 mg/kg following MAP induction and at a dose of 100 mg/kg following SAP induction. The serum levels of cytokines, lipase, and amylase were determined, and pancreatic and pulmonary tissues were harvested. Results. The serum levels of amylase, lipase, and cytokines were significantly decreased in both MAP and SAP models after Nar treatment. The malondialdehyde (MDA) levels of the pancreatic tissue was significantly reduced in both MAP and SAP after Nar treatment. In contrast, glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST), total sulfhydryl (T-SH), and non-proteinsulthydryl (NP-SH) were markedly increased in both MAP and SAP after Nar treatment. The injury in pancreatic and pulmonary tissues was markedly improved as evidenced by the inhibited expression of myeloperoxidase, nod-like receptor protein 3, and interleukin 1 beta as well as the enhanced expression of nuclear factor erythroid 2-related factor 2/heme oxygenase-1 in pancreatic tissues. Conclusions. Nar exerted protective effects on Cae-induced MAP and L-arginine-induced SAP in mice, suggesting that Nar may be a potential therapeutic intervention for AP.
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8

Hardman, J., C. Shields, D. Schofield, R. McMahon, H. P. Redmond, and A. K. Siriwardena. "Intravenous antioxidant modulation of end-organ damage in L-arginine-induced experimental acute pancreatitis." Pancreatology 5, no. 4-5 (2005): 380–86. http://dx.doi.org/10.1159/000086538.

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9

Szabolcs, Annamaria, Russel J. Reiter, Tamas Letoha, et al. "Effect of melatonin on the severity of L-arginine-induced experimental acute pancreatitis in rats." World Journal of Gastroenterology 12, no. 2 (2006): 251. http://dx.doi.org/10.3748/wjg.v12.i2.251.

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10

Frick, T. W., C. Fernández-del-Castillo, D. Bimmler, and A. L. Warshaw. "Elevated calcium and activation of trypsinogen in rat pancreatic acini." Gut 41, no. 3 (1997): 339–43. http://dx.doi.org/10.1136/gut.41.3.339.

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Background—Acute pancreatitis associated with hypercalcaemia has been described in humans and experimental animals. It has been demonstrated that calcium dose dependently accelerates trypsinogen activation, and it is generally believed that ectopic activation of digestive enzymes is an early event in the pathophysiology of acute pancreatitis.Aims and methods—Trypsinogen activation peptide (TAP) was measured in isolated rat pancreatic acini exposed to elevated extracellular calcium in order to investigate the association between calcium and trypsinogen activation in living cells. TAP was determined in the culture medium either before (extracellular compartment) or after (intracellular compartment) cell homogenisation.Results—Neither secretory stimulation nor elevated calcium alone caused an increase in TAP levels. Maximal cerulein or carbachol stimulation superimposed on high medium calcium, however, significantly increased intracellular trypsinogen activation twofold. This increase was inhibited by eitherNG-monomethyl-l-arginine (l-NMMA) or verapamil. Acinar cell morphology and function remained intact as demonstrated by electron microscopy and secretagogue dose-response studies.Conclusions—These results support the hypothesis that increased intracellular trypsinogen activation is an early step in the pathogenesis of hypercalcaemia induced pancreatitis. The model may have a bearing on other types of pancreatitis as elevated cytosolic calcium is thought to be an early event in the pathogenesis of acute pancreatitis in general.
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