Log in

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

To see the other types of publications on this topic, follow the link: Experimental acute pancreatitis ; L-arginine induced acute pancreatitis.

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

Author: Grafiati

Published: 4 June 2021

Last updated: 4 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Experimental acute pancreatitis ; L-arginine induced acute pancreatitis.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

11

Cikman, Oztekin, Omer Soylemez, Omer Faruk Ozkan, et al. "Antioxidant Activity of Syringic Acid Prevents Oxidative Stress in l-arginine–Induced Acute Pancreatitis: An Experimental Study on Rats." International Surgery 100, no. 5 (2015): 891–96. http://dx.doi.org/10.9738/intsurg-d-14-00170.1.

Full text

Abstract:

The aim of this study was to investigate the possible protective role of antioxidant treatment with syringic acid (SA) on l-arginine–induced acute pancreatitis (AP) using biochemical and histopathologic approaches. A total of 30 rats were divided into 3 groups. The control group received normal saline intraperitoneally. The AP group was induced by 3.2 g/kg body weight l-arginine intraperitoneally, administered twice with an interval of 1 hour between administrations. The AP plus SA group, after having AP induced by 3.2 g/kg body weight l-arginine, was given SA (50 mg kg−1) in 2 parts within 24 hours. The rats were killed, and pancreatic tissue was removed and used in biochemical and histopathologic examinations. Compared with the control group, the mean pancreatic tissue total oxidant status level, oxidative stress index, and lipid hydroperoxide levels were significantly increased in the AP group, being 30.97 ± 7.13 (P &lt; 0.05), 1.76 ± 0.34 (P &lt; 0.0001), and 19.18 ± 4.91 (P &lt; 0.01), respectively. However, mean total antioxidant status and sulfhydryl group levels were significantly decreased in the AP group compared with the control group, being 1.765 ± 0.21 (P &lt; 0.0001) and 0.21 ± 0.04 (P &lt; 0.0001), respectively. SA reduces oxidative stress markers and has antioxidant effects. It also augments antioxidant capacity in l-arginine–induced acute toxicity of pancreas in rats.

APA, Harvard, Vancouver, ISO, and other styles

12

Mirmalek, Seyed Abbas, Ala Gholamrezaei Boushehrinejad, Hassan Yavari, et al. "Antioxidant and Anti-Inflammatory Effects of Coenzyme Q10 on L-Arginine-Induced Acute Pancreatitis in Rat." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/5818479.

Full text

Abstract:

This study was aimed at evaluating the protective effect of coenzyme Q10 on L-arginine-induced acute pancreatitis in rats regarding biomarkers and morphologic changes. Thirty-two male Sprague-Dawley rats were divided into 4 equal groups. Control group received intraperitoneal normal saline, while in sham and experimental groups 1 and 2 pancreatitis was induced with L-arginine. E1 and E2 groups were treated with a single dose of 100 and 200 mg/kg Q10, respectively. Serum lipase and amylase, along with pancreas IL-10, IL-1β, and TNF-α, were measured. For evaluation of oxidative stress, pancreatic superoxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA), and myeloperoxidase (MPO) were assessed. Histopathological examination for morphologic investigation was conducted. Serum amylase and lipase, as well as TNF-αand IL-1βcytokines, reverted with administration of Q10 in consistence with dosage. In contrast, Q10 assisted in boosting of IL-10 with higher dosage (200 mg/kg). A similar pattern for oxidative stress markers was noticed. Both MDA and MPO levels declined with increased dosage, contrary to elevation of SOD and GSH. Histopathology was in favor of protective effects of Q10. Our findings proved the amelioration of pancreatic injury by Q10, which suggest the anti-inflammatory and antioxidant property of Q10 and its potential therapeutic role.

APA, Harvard, Vancouver, ISO, and other styles

13

Gulturk, Baris, Ahmet Bozdag, Refik Ayten, et al. "Effects of sildenafil citrate on pancreatic and lung complications in an experimental L-arginine-induced acute pancreatitis model." Gastroenterology Review 16, no. 1 (2021): 29–35. http://dx.doi.org/10.5114/pg.2021.104734.

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

Farghaly, Lamia M., Nagwan A. Sabak, and Naglaa A. El-sherbeny. "The protective effect of L-tryptophan versus alpha lipoic acid against L-arginine-induced experimental acute pancreatitis in albino rats." Egyptian Journal of Hospital Medicine 26, no. 1 (2007): 31–45. http://dx.doi.org/10.21608/ejhm.2007.17778.

Full text

APA, Harvard, Vancouver, ISO, and other styles

15

Bálint, Emese Réka, Zsolt Balla, Balázs Kui, et al. "Fentanyl impairs the severity of L-ornithine-induced experimental acute pancreatitis in rats." Pancreatology 18, no. 4 (2018): S28. http://dx.doi.org/10.1016/j.pan.2018.05.075.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

Al-Mufti, R. A., R. C. N. Williamson, and R. T. Mathie. "Increased nitric oxide activity in a rat model of acute pancreatitis." Gut 43, no. 4 (1998): 564–70. http://dx.doi.org/10.1136/gut.43.4.564.

Full text

Abstract:

Background—Overproduction of nitric oxide (NO) via induction of the inducible NO synthase (iNOS) is an important factor in the haemodynamic disturbances of several inflammatory states.Aims—To identify the role of NO in a caerulein induced model of acute pancreatitis in the rat.Methods—Arterial blood pressure and plasma NO metabolites were measured at zero and seven hours in adult male Wistar rats administered caerulein (n=10) or saline (n=10). Pancreatic activity of NOS (inducible and constitutive) was assayed biochemically. The pancreatic expression and cellular localisation of NOS and nitrotyrosine (a marker of peroxynitrite induced oxidative tissue damage) were characterised immunohistochemically.Results—Compared with controls at seven hours, the pancreatitis group displayed raised plasma NO metabolites (mean (SEM) 70.2 (5.9) versus 22.7 (2.2) μmol/l, p<0.0001) and reduced mean arterial blood pressure (88.7 (4.6) versus 112.8 (4.1) mm Hg, p=0.008). There was notable iNOS activity in the pancreatitis group (3.1 (0.34) versus 0.1 (0.01) pmol/mg protein/min, p<0.0001) with reduced constitutive NOS activity (0.62 (0.12) versus 0.96 (0.08) pmol/mg protein/min, p=0.031). The increased expression of iNOS was mainly localised within vascular smooth muscle cells (p=0.003 versus controls), with positive perivascular staining for nitrotyrosine (p=0.0012 versus controls).Conclusions—In this experimental model of acute pancreatitis, iNOS induction and oxidative tissue damage in the pancreas is associated with raised systemic NO and arterial hypotension. Excess production of NO arising from the inducible NO synthase may be an important factor in the systemic and local haemodynamic disturbances associated with acute pancreatitis.

APA, Harvard, Vancouver, ISO, and other styles

17

Hegyi, Peter, Tamas Takacs, Norbert Farkas, et al. "Insulin is necessary for the hypertrophic effect of CCK-8 following acute necrotizing experimental pancreatitis induced by L-Arginine in diabetic rats." Gastroenterology 118, no. 4 (2000): A650—A651. http://dx.doi.org/10.1016/s0016-5085(00)84741-1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

Lin, Ziqi, Chenlong Zhang, Xiaoxin Zhang, et al. "Improving Small Intestinal Motility in Experimental Acute Necrotising Pancreatitis by Modulating the CPI-17/MLCP Pathway Using Chaiqin Chengqi Decoction." Evidence-Based Complementary and Alternative Medicine 2020 (February 10, 2020): 1–14. http://dx.doi.org/10.1155/2020/9189457.

Full text

Abstract:

Protein kinase C-potentiated inhibitor protein of 17 kDa (CPI-17), a specific inhibitor of myosin light-chain phosphatase (MLCP) regulated by proinflammatory cytokines, is central for calcium sensitisation. We investigated the effects of chaiqin chengqi decoction (CQCQD) on the CPI-17/MLCP pathway in the small intestinal smooth muscle cells (SMCs) and strips (SMS) in an AP model. Necrotising AP was induced in rats by intraperitoneal injections (IPI) of L-ornithine (3.0 g/kg, pH 7.0; hourly × 2) at 1 hour apart; controls received saline. In treatment groups, carbachol (CCh; 60 μg/kg, IPI) or CQCQD (20 g/kg; 2-hourly × 3, intragastric) was administered. The necrotising AP model was associated with systemic inflammation (serum IL-1β and TNF-α) and worsened jejunum histopathology and motility (serum vasoactive intestinal peptide and intestinal fatty acid-binding protein) as the disease progressed. There was decreased intracellular calcium concentration ([Ca2+]i) SMCs. Contractile function of isolated SMCs was reduced and associated with down-regulated expression of key mRNAs and proteins of the CPI-17/MLCP pathway as well as increased IL-1β and TNF-α. CQCQD and CCh significantly reversed these changes and the disease severity. These data suggest that CQCQD can improve intestinal motility by modulating the CPI-17/MLCP pathway in small intestinal smooth muscle during AP.

APA, Harvard, Vancouver, ISO, and other styles

19

Tachibana, I., T. Akiyama, K. Kanagawa, et al. "Defect in pancreatic exocrine and endocrine response to CCK in genetically diabetic OLETF rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 270, no. 4 (1996): G730—G737. http://dx.doi.org/10.1152/ajpgi.1996.270.4.g730.

Full text

Abstract:

Clinical as well as experimental studies in insulinopenic diabetes mellitus have demonstrated abnormal pancreatic exocrine responses to cholecystokinin (CCK). In the present study, we examined pancreatic exocrine and endocrine function in the recently developed genetically diabetic Otsuka Long-Evans Tokushima fatty (OLETF) rats and compared them with those in the control Long-Evans Tokushima Otsuka (LETO) rats of the same age. Stepwise increasing doses of CCK octapeptide (CCK-8; 0.027-7.0 nmol.kg-1.h-1) evoked a characteristic biphasic dose-response curve for pancreatic juice and protein output in the LETO rats, whereas the OLETF rats were totally insensitive to CCK-8 stimulation. However, the responsiveness and the sensitivity to both carbamylcholine and secretin were similar in the two groups. Intraduodenal infusion of casein (500 mg/h) failed to stimulate pancreatic exocrine secretion in the OLETF rats despite a greater CCK response than in the LETO rats (peak response: 8.43 +/- 0.97 vs 5.12 +/- 0.30 pmol/l in LETO, P < 0.01). Intravenous infusion of CCK-8 (4.4 nmol.kg-1.20 min-1) caused a significant increase in serum insulin concentrations and a concomitant decrease in glucose levels in the LETO rats but not in the OLETF rats. On the other hand, an intravenous bolus injection of 1.1 mmol/kg glucose caused a greater insulin release in the OLETF rats than in the LETO rats. In contrast, gastric acid secretion in the OLETF rats was significantly high in basal and in response to intravenous infusion of CCK-8 compared with that in the LETO rats. Four subcutaneous injections of 20 micrograms/kg caerulein at hourly intervals over 3 h induced acute pancreatitis in the LETO rats but did not elicit any significant increase in serum amylase or lipase activities and pancreatic wet weight or histological evidence of acute pancreatitis in the OLETF rats. These results indicate that the exocrine and endocrine pancreas of the recently developed genetically diabetic OLETF rats are totally and specifically insensitive to exogenous and endogenous CCK stimulation, whereas parietal cells in these rats are sensitive to CCK stimulation.

APA, Harvard, Vancouver, ISO, and other styles

20

Kui, Balazs, Zsolt Balla, Peter Hegyi, and Zoltan Rakonczay. "L-arginine-induced acute pancreatitis in mice: Revisited." Pancreatology 13, no. 3 (2013): S21—S22. http://dx.doi.org/10.1016/j.pan.2013.04.066.

Full text

APA, Harvard, Vancouver, ISO, and other styles

21

Zhang, Zhiqiang, Yanqing Wang, Ming Dong, Jianchun Cui, Daqing Rong, and Qi Dong. "Oxymatrine Ameliorates l-Arginine-Induced Acute Pancreatitis in Rats." Inflammation 35, no. 2 (2011): 605–13. http://dx.doi.org/10.1007/s10753-011-9352-2.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Uçmak, Feyzullah, Nazım Ekin, İbrahim İbiloğlu, Serkan Arslan, İbrahim Kaplan, and Ebubekir Şenateş. "Prophylactic Administration of Silybin Ameliorates L-Arginine-Induced Acute Pancreatitis." Medical Science Monitor 22 (October 11, 2016): 3641–46. http://dx.doi.org/10.12659/msm.898014.

Full text

APA, Harvard, Vancouver, ISO, and other styles

23

Yenicerioglu, Akan, Ziya Cetinkaya, Mustafa Girgin, et al. "Effects of trimetazidine in acute pancreatitis induced by L-arginine." Canadian Journal of Surgery 56, no. 3 (2013): 175–79. http://dx.doi.org/10.1503/cjs.032811.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

Kui, Balázs, Zsolt Balla, Béla Vasas, et al. "New Insights into the Methodology of L-Arginine-Induced Acute Pancreatitis." PLOS ONE 10, no. 2 (2015): e0117588. http://dx.doi.org/10.1371/journal.pone.0117588.

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

Kaur, Jagdeep, Shabir Sidhu, Kanwaljit Chopra, and M. U. Khan. "Calendula officinalis ameliorates l-arginine-induced acute necrotizing pancreatitis in rats." Pharmaceutical Biology 54, no. 12 (2016): 2951–59. http://dx.doi.org/10.1080/13880209.2016.1195848.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Chen, Ji, Qing-ping Cai, Pi-jie Shen, et al. "Netrin-1 Protects against L-Arginine-Induced Acute Pancreatitis in Mice." PLoS ONE 7, no. 9 (2012): e46201. http://dx.doi.org/10.1371/journal.pone.0046201.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Cheng, Li, Zhenguo Qiao, Chunfang Xu, and Jiaqing Shen. "Midkine is overexpressed in acute pancreatitis and promotes the pancreatic recovery in L‐arginine‐induced acute pancreatitis in mice." Journal of Gastroenterology and Hepatology 32, no. 6 (2017): 1265–72. http://dx.doi.org/10.1111/jgh.13681.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

ISHIWATA, Toshiyuki, Mitsuhiro KUDO, Munehiko ONDA, et al. "Defined localization of nestin-expressing cells in l-arginine-induced acute pancreatitis." Suizo 21, no. 6 (2006): 539–41. http://dx.doi.org/10.2958/suizo.21.539.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

Ishiwata, Toshiyuki, Mitsuhiro Kudo, Munehiko Onda, et al. "Defined Localization of Nestin-expressing Cells in l-arginine-induced Acute Pancreatitis." Pancreas 32, no. 4 (2006): 360–68. http://dx.doi.org/10.1097/01.mpa.0000220860.01120.21.

Full text

APA, Harvard, Vancouver, ISO, and other styles

30

Jin, T., L. Wen, M. A. Javed, et al. "Caffeine does not protect against L-arginine-induced acute pancreatitis in mice." Pancreatology 13, no. 2 (2013): e40. http://dx.doi.org/10.1016/j.pan.2012.12.195.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

Sanz Martín, P., M. P. Hernández Lorenzo, J. I. San Román García, J. J. Calvo Andrés, and M. García Benito. "Alterations in ductal secretion in L-arginine induced acute pancreatitis in rats." Pancreatology 13, no. 4 (2013): e11. http://dx.doi.org/10.1016/j.pan.2013.07.039.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Guo, Fei, Shutao Zheng, Xiaokang Gao, Qiong Zhang, and Jiangwei Liu. "A Novel Acute Necrotizing Pancreatitis Model Induced by L-Arginine in Rats." Pancreas 44, no. 2 (2015): 279–86. http://dx.doi.org/10.1097/mpa.0000000000000259.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Biczó, György, Péter Hegyi, Sándor Berczi, et al. "Inhibition of Arginase Activity Ameliorates L-Arginine-Induced Acute Pancreatitis in Rats." Pancreas 39, no. 6 (2010): 868–74. http://dx.doi.org/10.1097/mpa.0b013e3181d371f8.

Full text

APA, Harvard, Vancouver, ISO, and other styles

34

Aziz, N. M., M. Y. Kamel, and R. A. Rifaai. "Eff ects of hemin, a heme oxygenase-1 inducer in L-arginine-induced acute pancreatitis and associated lung injury in adult male albino rats." Endocrine Regulations 51, no. 1 (2017): 20–30. http://dx.doi.org/10.1515/enr-2017-0003.

Full text

Abstract:

AbstractObjective. The aim of the current study was to assess the protective outcome of hemin, a heme oxygenase-1 (HO-1) inducer on L-arginine-induced acute pancreatitis in rats. Acute pancreatitis (AP) is considered to be a critical inflammatory disorder with a major impact on the patient health. Various theories have been recommended regarding the pathophysiology of AP and associated pulmonary complications.Methods. Twenty-four adult male albino rats were randomly divided into four groups: control group, acute pancreatitis (AP), hemin pre-treated AP group, and hemin post-treated AP group.Results. Administration of hemin before induction of AP significantly attenuated the L-arginine- induced pancreatitis and associated pulmonary complications characterized by the increasing serum levels of amylase, lipase, tumor necrosis factor-α, nitric oxide, and histo-architectural changes in pancreas and lungs as compared to control group. Additionally, pre-treatment with hemin significantly compensated the deficits in total antioxidant capacities and lowered the elevated malondialdehyde levels observed with AP. On the other hand, post-hemin administration did not show any protection against L-arginine-induced AP.Conclusions. The current study indicates that the induction of HO-1 by hemin pre-treatment significantly ameliorated the L-arginine-induced pancreatitis and associated pulmonary complications may be due to its anti-inflammatory and antioxidant properties.

APA, Harvard, Vancouver, ISO, and other styles

35

Binet, Quentin, Inès Dufour, Emmanuel Agneessens, et al. "The second case of a young man with l-arginine-induced acute pancreatitis." Clinical Journal of Gastroenterology 11, no. 5 (2018): 424–27. http://dx.doi.org/10.1007/s12328-018-0862-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

36

Werner, J., C. Fernández-del Castillo, J. A. Rivera, et al. "On the protective mechanisms of nitric oxide in acute pancreatitis." Gut 43, no. 3 (1998): 401–7. http://dx.doi.org/10.1136/gut.43.3.401.

Full text

Abstract:

Background—Ectopic protease activation, microcirculatory changes, and leucocyte activation are the main events in the pathogenesis of acute pancreatitis. Nitric oxide (NO) is known to be a key mediator in the normal and inflamed pancreas.Aims—To investigate the targets on which NO exerts its effect in caerulein induced pancreatitis.Methods—Acute pancreatitis was induced in rats which additionally received either the NO synthase substrate, l-arginine; the NO donor, sodium nitroprusside; or the NO synthase inhibitor, N-nitro-l-arginine methyl ester (l-NAME). At six hours, pancreatic injury (oedema, leucocyte content, ectopic trypsinogen activation) was analysed and pancreatic oxygenation and perfusion were determined. A direct influence of NO on amylase secretion and trypsinogen activation was evaluated separately in vitro.Results—Both NO donors reduced the grade of inflammation. l-NAME increased the severity of inflammation, while decreasing pancreatic tissue oxygenation. Although neither amylase secretion nor intracellular trypsinogen activation in caerulein stimulated pancreatic acini was influenced by either NO donors or inhibitors, both NO donors decreased intrapancreatic trypsinogen activation peptide (TAP) and pancreatic oedema in vivo, andl-NAME increased TAP.Conclusions—NO protects against injury caused by pancreatitis in the intact animal but has no discernible effect on isolated acini. It is likely that in pancreatitis NO acts indirectly via microcirculatory changes, including inhibition of leucocyte activation and preservation of capillary perfusion.

APA, Harvard, Vancouver, ISO, and other styles

37

Takács, Tamás, Zoltán Rakonczay Jr., Ilona S. Varga, et al. "Comparative effects of water immersion pretreatment on three different acute pancreatitis models in rats." Biochemistry and Cell Biology 80, no. 2 (2002): 241–51. http://dx.doi.org/10.1139/o02-006.

Full text

Abstract:

Cells respond to stress by upregulating the synthesis of cytoprotective heat shock proteins (HSPs) and antioxidant enzymes. The aim of this study was to compare the effects of cold (CWI) or hot water immersion (HWI) stress on three different acute pancreatitis models (cholecystokinin octapeptide (CCK), sodium taurocholate (TC), and L-arginine (Arg)). We examined the levels of pancreatic HSP60, HSP72, and antioxidants after the water immersion stress. Male Wistar rats were injected with CCK, TC, or Arg at the peak level of pancreatic HSP synthesis, as determined by Western blot analysis. HWI significantly elevated HSP72 expression and CWI significantly increased HSP60 expression in the pancreas. Water immersion stress decreased the levels of pancreatic antioxidants. CWI and HWI pretreatment ameliorated most of the examined laboratory and morphological parameters of CCK-induced pancreatitis. CWI pretreatment decreased pancreatic edema and the serum amylase level; however, the morphological damage was more severe in TC-induced acute pancreatitis. Overall, CWI and HWI pretreatment only decreased the serum cytokine concentrations in Arg-induced pancreatitis. CWI and HWI resulted in differential induction of pancreatic HSP60 and HSP72 and the depletion of antioxidants. The findings suggest the possible roles of HSP60 and (or) HSP72 (but not that of the antioxidant enzymes) in the protection against CCK- and TC-induced acute pancreatitis. Unexpectedly, CWI pretreatment was detrimental to the morphological parameters of TC-induced pancreatitis. It was demonstrated that CWI and HWI pretreatment only influenced cytokine synthesis in Arg-induced pancreatitis.Key words: heat shock proteins, water immersion, cholecystokinin octapeptide, sodium taurocholate, L-arginine, pancreatitis.

APA, Harvard, Vancouver, ISO, and other styles

38

Elder, Alison S. F., Gino T. P. Saccone, Andrew D. Bersten, and Dani-Louise Dixon. "L-Arginine–induced acute pancreatitis results in mild lung inflammation without altered respiratory mechanics." Experimental Lung Research 37, no. 1 (2010): 1–9. http://dx.doi.org/10.3109/01902148.2010.495822.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

Melo, Caroline Mourão. "α,β-amyrin, a natural triterpenoid ameliorates L-arginine-induced acute pancreatitis in rats". World Journal of Gastroenterology 16, № 34 (2010): 4272. http://dx.doi.org/10.3748/wjg.v16.i34.4272.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Czakó, László, Tamás Takács, Ilona Sz Varga, et al. "The pathogenesis of L-arginine-induced acute necrotizing pancreatitis: Inflammatory mediators and endogenous cholecystokinin." Journal of Physiology-Paris 94, no. 1 (2000): 43–50. http://dx.doi.org/10.1016/s0928-4257(99)00104-7.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

Onur, Ender, Melih Paksoy, Bilgi Baca, and Haldun Akoglu. "Hyperbaric Oxygen and N-Acetylcysteine Treatment in L-Arginine-Induced Acute Pancreatitis in Rats." Journal of Investigative Surgery 25, no. 1 (2011): 20–28. http://dx.doi.org/10.3109/08941939.2011.593694.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Takács, Tamás, László Czakó, Éva Morschl, et al. "The Role of Nitric Oxide in Edema Formation in L-Arginine-Induced Acute Pancreatitis." Pancreas 25, no. 3 (2002): 277–82. http://dx.doi.org/10.1097/00006676-200210000-00010.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

Chen, Han, Yan Ping Sun, Yang Li, et al. "Hydrogen-rich saline ameliorates the severity of l-arginine-induced acute pancreatitis in rats." Biochemical and Biophysical Research Communications 393, no. 2 (2010): 308–13. http://dx.doi.org/10.1016/j.bbrc.2010.02.005.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

Merza, Mohammed, Milladur Rahman, Songen Zhang, et al. "Human thrombin-derived host defense peptides inhibit neutrophil recruitment and tissue injury in severe acute pancreatitis." American Journal of Physiology-Gastrointestinal and Liver Physiology 307, no. 9 (2014): G914—G921. http://dx.doi.org/10.1152/ajpgi.00237.2014.

Full text

Abstract:

Severe acute pancreatitis (AP) is characterized by leukocyte infiltration and tissue injury. Herein, we wanted to examine the potential effects of thrombin-derived host defense peptides (TDPs) in severe AP. Pancreatitis was provoked by infusion of taurocholate into the pancreatic duct or by intraperitoneal administration of l-arginine in C57BL/6 mice. Animals were treated with the TDPs GKY20 and GKY25 or a control peptide WFF25 30 min before induction of AP. TDPs reduced blood amylase levels, neutrophil infiltration, hemorrhage, necrosis, and edema formation in the inflamed pancreas. Treatment with TDPs markedly attenuated the taurocholate-induced increase in plasma levels of CXCL2 and interleukin-6. Moreover, administration of TDPs decreased histone 3, histone 4, and myeloperoxidase levels in the pancreas in response to taurocholate challenge. Interestingly, administration of TDPs abolished neutrophil expression of Mac-1 in mice with pancreatitis. In addition, TDPs inhibited CXCL2-induced chemotaxis of isolated neutrophils in vitro. Fluorescent-labeled TDP was found to directly bind to isolated neutrophils. Finally, a beneficial effect of TDPs was confirmed in l-arginine-induced pancreatitis. Our novel results demonstrate that TDPs exert protective effects against pathological inflammation and tissue damage in AP. These findings suggest that TDPs might be useful in the management of patients with severe AP.

APA, Harvard, Vancouver, ISO, and other styles

45

Al-Hariri, Mohammed T., Tharwat G. Eldin, Tarek Hashim, Shahanas Chathoth, and Abdullah Alswied. "Propolis Modulates Inflammatory Mediators and Improves Histopathology in Male Rats with L-arginine-induced Acute Pancreatitis." Sultan Qaboos University Medical Journal [SQUMJ] 19, no. 2 (2019): 103. http://dx.doi.org/10.18295/squmj.2019.19.02.004.

Full text

Abstract:

ABSTRACT: Objectives: This study aimed to determine the effects of propolis on immune mediators and tissue histopathology in rats with L-arginine-induced acute pancreatitis (AP). Methods: This study was conducted at Imam Abdulrahman Bin Faisal University, Dammam, Saudia Arabia between September and November 2017. A total of 24 male albino Wistar rats were divided into three equal groups. Group one was the negative control, group two was the positive control (L-arginine-induced AP) and group three received treatment (L-arginineinduced AP and propolis). The rats in group three were treated with 100 mg/kg propolis for seven days after AP induction. Pancreatic tissue was evaluated histologically and levels of interleukin (IL)-6, IL-22 and IL-1β and tumour necrosis factor-alpha (TNF-α) were measured. Results: Propolis reduced the quanitity of proinflammatory molecules (TNF-α, IL-1β and IL-6) in group three compared to group two, significantly increased the overall anti-inflammatory effect of IL-22 (P <0.005) and reduced interstitial inflammation and neutrophil cell infiltration of the pancreatic tissues. Conclusion: Propolis may exert a therapeutic effect in AP. Further studies are required to demonstrate the mechanisms of propolis in AP.Keywords: Propolis; Arginine; Pancreatitis; Interleukins; Cytokinesis; Rats; Saudi Arabia.

APA, Harvard, Vancouver, ISO, and other styles

46

Hamouda, Hala, Ahmed Abd-Allah, Ghada Abd El Alem, Omnia El-Deeb, and Kareema El-Desoky. "Effect of Melatonin on some Inflammatory Markers in L-arginine Induced acute Pancreatitis in Rats." Bulletin of Egyptian Society for Physiological Sciences 31, no. 1 (2011): 147–64. http://dx.doi.org/10.21608/besps.2011.35978.

Full text

APA, Harvard, Vancouver, ISO, and other styles

47

Biradar, Sandeep, and Veeresh B. "Pre-Clinical Evolutionary Study of Alpha-Pinene in L-Arginine Induced Acute Pancreatitis in Rat." Indian Journal Of Pharmaceutical Education And Research 47, no. 4 (2014): 73–78. http://dx.doi.org/10.5530/ijper.47.4.10.

Full text

APA, Harvard, Vancouver, ISO, and other styles

48

Reddy, S. H. S., T. G. Jacob, P. K. Garg, and P. Sahni. "Effect of dexamethasone and infliximab on the severity of L-arginine induced murine acute pancreatitis." HPB 20 (September 2018): S209. http://dx.doi.org/10.1016/j.hpb.2018.06.083.

Full text

APA, Harvard, Vancouver, ISO, and other styles

49

Naito, Zenya, Toshiyuki Ishiwata, Yue Ping Lu, et al. "Transient and ectopic expression of lumican by acinar cells in l-arginine-induced acute pancreatitis." Experimental and Molecular Pathology 74, no. 1 (2003): 33–39. http://dx.doi.org/10.1016/s0014-4800(03)80006-0.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Shen, Jiaqing, Rong Wan, Guoyong Hu, Feng Wang, Jie Shen, and Xingpeng Wang. "Involvement of thrombopoietin in acinar cell necrosis in l-arginine-induced acute pancreatitis in mice." Cytokine 60, no. 1 (2012): 294–301. http://dx.doi.org/10.1016/j.cyto.2012.05.005.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!