Effects of glucocorticoid agonist and antagonist on the pathogenesis of L-arginine-induced acute pancreatitis in rat

Attila Paszt, Katalin Éder, Annamária Szabolcs, L. Tiszlavicz, György Lázár, E. Duda, T. Takács, G. Lazar

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

OBJECTIVES: To investigate the consequences of treatment with an exogenous glucocorticoid agonist (methylprednisolone) and antagonist (RU-38486) on the local and systemic responses in l-arginine-induced acute pancreatitis in rats. METHODS: The methylprednisolone and RU-38486 were administered just before pancreatitis induction. Plasma amylase activity, interleukin 6 activity, pancreatic weight/body weight ratio, plasma macrophage migration inhibitory factor (MIF) concentration, and pancreatic nuclear transcription factor (NF) κB activity were determined. The extents of pancreas, liver, and lung injuries were assessed by histology. RESULTS: Acute pancreatitis resulted in NF-κB activation and proinflammatory cytokine release in rats. In the glucocorticoid agonist group, plasma amylase and interleukin 6 levels were significantly decreased as compared with those of RU-38486 and nontreated groups. Antagonist treatment led to significantly higher MIF production at 8 and 12 hours after l-arginine injection as compared with the agonist-treated and nontreated groups. Glucocorticoid agonist treatment significantly decreased the level of NF-κB 24 hours after pancreatitis induction. Histological investigations showed protective effect of agonist treatment on acute pancreatitis-induced tissue damage in the pancreas and lung. CONCLUSIONS: These results corroborated the importance of MIF in acute pancreatitis. The glucocorticoid-dependent mechanisms seem to play a crucial role in the control of the inflammatory response and tissue damage in l-arginine-induced experimental acute pancreatitis.

Original languageEnglish
Pages (from-to)369-376
Number of pages8
JournalPancreas.
Volume36
Issue number4
DOIs
Publication statusPublished - May 2008

Fingerprint

Pancreatitis
Glucocorticoids
Arginine
Mifepristone
Transcription Factors
Methylprednisolone
Amylases
Pancreas
Interleukin-6
Macrophage Migration-Inhibitory Factors
Lung Injury
Therapeutics
Histology
Body Weight
Cytokines
Weights and Measures
Lung
Injections
Liver

Keywords

  • Experimental pancreatitis
  • Glucocorticoid hormones
  • MIF
  • NF-κB
  • Organ failure

ASJC Scopus subject areas

  • Gastroenterology
  • Endocrinology

Cite this

Effects of glucocorticoid agonist and antagonist on the pathogenesis of L-arginine-induced acute pancreatitis in rat. / Paszt, Attila; Éder, Katalin; Szabolcs, Annamária; Tiszlavicz, L.; Lázár, György; Duda, E.; Takács, T.; Lazar, G.

In: Pancreas., Vol. 36, No. 4, 05.2008, p. 369-376.

Research output: Contribution to journalArticle

@article{7b9085e5a5624522bb05bf3f89431ec6,
title = "Effects of glucocorticoid agonist and antagonist on the pathogenesis of L-arginine-induced acute pancreatitis in rat",
abstract = "OBJECTIVES: To investigate the consequences of treatment with an exogenous glucocorticoid agonist (methylprednisolone) and antagonist (RU-38486) on the local and systemic responses in l-arginine-induced acute pancreatitis in rats. METHODS: The methylprednisolone and RU-38486 were administered just before pancreatitis induction. Plasma amylase activity, interleukin 6 activity, pancreatic weight/body weight ratio, plasma macrophage migration inhibitory factor (MIF) concentration, and pancreatic nuclear transcription factor (NF) κB activity were determined. The extents of pancreas, liver, and lung injuries were assessed by histology. RESULTS: Acute pancreatitis resulted in NF-κB activation and proinflammatory cytokine release in rats. In the glucocorticoid agonist group, plasma amylase and interleukin 6 levels were significantly decreased as compared with those of RU-38486 and nontreated groups. Antagonist treatment led to significantly higher MIF production at 8 and 12 hours after l-arginine injection as compared with the agonist-treated and nontreated groups. Glucocorticoid agonist treatment significantly decreased the level of NF-κB 24 hours after pancreatitis induction. Histological investigations showed protective effect of agonist treatment on acute pancreatitis-induced tissue damage in the pancreas and lung. CONCLUSIONS: These results corroborated the importance of MIF in acute pancreatitis. The glucocorticoid-dependent mechanisms seem to play a crucial role in the control of the inflammatory response and tissue damage in l-arginine-induced experimental acute pancreatitis.",
keywords = "Experimental pancreatitis, Glucocorticoid hormones, MIF, NF-κB, Organ failure",
author = "Attila Paszt and Katalin {\'E}der and Annam{\'a}ria Szabolcs and L. Tiszlavicz and Gy{\"o}rgy L{\'a}z{\'a}r and E. Duda and T. Tak{\'a}cs and G. Lazar",
year = "2008",
month = "5",
doi = "10.1097/MPA.0b013e31815bd26a",
language = "English",
volume = "36",
pages = "369--376",
journal = "Pancreas",
issn = "0885-3177",
publisher = "Lippincott Williams and Wilkins",
number = "4",

}

TY - JOUR

T1 - Effects of glucocorticoid agonist and antagonist on the pathogenesis of L-arginine-induced acute pancreatitis in rat

AU - Paszt, Attila

AU - Éder, Katalin

AU - Szabolcs, Annamária

AU - Tiszlavicz, L.

AU - Lázár, György

AU - Duda, E.

AU - Takács, T.

AU - Lazar, G.

PY - 2008/5

Y1 - 2008/5

N2 - OBJECTIVES: To investigate the consequences of treatment with an exogenous glucocorticoid agonist (methylprednisolone) and antagonist (RU-38486) on the local and systemic responses in l-arginine-induced acute pancreatitis in rats. METHODS: The methylprednisolone and RU-38486 were administered just before pancreatitis induction. Plasma amylase activity, interleukin 6 activity, pancreatic weight/body weight ratio, plasma macrophage migration inhibitory factor (MIF) concentration, and pancreatic nuclear transcription factor (NF) κB activity were determined. The extents of pancreas, liver, and lung injuries were assessed by histology. RESULTS: Acute pancreatitis resulted in NF-κB activation and proinflammatory cytokine release in rats. In the glucocorticoid agonist group, plasma amylase and interleukin 6 levels were significantly decreased as compared with those of RU-38486 and nontreated groups. Antagonist treatment led to significantly higher MIF production at 8 and 12 hours after l-arginine injection as compared with the agonist-treated and nontreated groups. Glucocorticoid agonist treatment significantly decreased the level of NF-κB 24 hours after pancreatitis induction. Histological investigations showed protective effect of agonist treatment on acute pancreatitis-induced tissue damage in the pancreas and lung. CONCLUSIONS: These results corroborated the importance of MIF in acute pancreatitis. The glucocorticoid-dependent mechanisms seem to play a crucial role in the control of the inflammatory response and tissue damage in l-arginine-induced experimental acute pancreatitis.

AB - OBJECTIVES: To investigate the consequences of treatment with an exogenous glucocorticoid agonist (methylprednisolone) and antagonist (RU-38486) on the local and systemic responses in l-arginine-induced acute pancreatitis in rats. METHODS: The methylprednisolone and RU-38486 were administered just before pancreatitis induction. Plasma amylase activity, interleukin 6 activity, pancreatic weight/body weight ratio, plasma macrophage migration inhibitory factor (MIF) concentration, and pancreatic nuclear transcription factor (NF) κB activity were determined. The extents of pancreas, liver, and lung injuries were assessed by histology. RESULTS: Acute pancreatitis resulted in NF-κB activation and proinflammatory cytokine release in rats. In the glucocorticoid agonist group, plasma amylase and interleukin 6 levels were significantly decreased as compared with those of RU-38486 and nontreated groups. Antagonist treatment led to significantly higher MIF production at 8 and 12 hours after l-arginine injection as compared with the agonist-treated and nontreated groups. Glucocorticoid agonist treatment significantly decreased the level of NF-κB 24 hours after pancreatitis induction. Histological investigations showed protective effect of agonist treatment on acute pancreatitis-induced tissue damage in the pancreas and lung. CONCLUSIONS: These results corroborated the importance of MIF in acute pancreatitis. The glucocorticoid-dependent mechanisms seem to play a crucial role in the control of the inflammatory response and tissue damage in l-arginine-induced experimental acute pancreatitis.

KW - Experimental pancreatitis

KW - Glucocorticoid hormones

KW - MIF

KW - NF-κB

KW - Organ failure

UR - http://www.scopus.com/inward/record.url?scp=42549152796&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=42549152796&partnerID=8YFLogxK

U2 - 10.1097/MPA.0b013e31815bd26a

DO - 10.1097/MPA.0b013e31815bd26a

M3 - Article

C2 - 18437083

AN - SCOPUS:42549152796

VL - 36

SP - 369

EP - 376

JO - Pancreas

JF - Pancreas

SN - 0885-3177

IS - 4

ER -