title: The role of the glucocorticoid-dependent mechanism in the progression of sodium taurocholate-induced acute pancreatitis in the rat.
abstract: The effects of glucocorticoids on acute pancreatitis (AP) have remained contradictory. The aim of this study was to investigate the time courses of the effects of the exogenous glucocorticoid agonists dexamethasone (DEX) and hydrocortisone (HYD) and a glucocorticoid antagonist (RU-38486) and to characterize the local and systemic responses in AP in rats. The glucocorticoid antagonist and agonists were administered just before AP induction. Serum amylase activity determinations, IL-6 bioassays, pancreatic weight/body weight ratio measurements, and survival analysis were performed. Liver and lung injuries were assessed via neutrophil leukocyte infiltration in myeloperoxidase (MPO) assays, tissue adenosine triphosphate (ATP) level determinations, and histology. In the glucocorticoid agonist groups, the survival rate increased, while the serum amylase level, the IL-6 activity, and the pancreatic weight/body weight ratio decreased significantly as compared with the control and RU-treated groups. AP resulted in significant decreases in tissue ATP levels in both the liver and the lung. In the DEX- or HYD-treated groups, the liver ATP levels were significantly elevated, while both the liver and the lung MPO levels were attenuated as compared with the AP and RU-treated groups. These results suggest that glucocorticoids may play important roles in mitigating the progression of the inflammatory reaction during the early phases of AP.
authors.affiliation: Department of Surgery, University of Szeged, Szeged, Hungary. pt@surg.szote.u-szeged.hu
authors.forename: A
authors.initials: A
authors.lastname: Paszt
authors.forename: T
authors.initials: T
authors.lastname: Takács
authors.forename: Z
authors.initials: Z
authors.lastname: Rakonczay
authors.forename: J
authors.initials: J
authors.lastname: Kaszaki
authors.forename: A
authors.initials: A
authors.lastname: Wolfard
authors.forename: L
authors.initials: L
authors.lastname: Tiszlavicz
authors.forename: G
authors.initials: G
authors.lastname: Lázár
authors.forename: E
authors.initials: E
authors.lastname: Duda
authors.forename: K
authors.initials: K
authors.lastname: Szentpáli
authors.forename: L
authors.initials: L
authors.lastname: Czakó
authors.forename: M
authors.initials: M
authors.lastname: Boros
authors.forename: A
authors.initials: A
authors.lastname: Balogh
authors.forename: G
authors.initials: G
authors.lastname: Lázár
mesh_terms: D000208:Acute Disease; D000255:Adenosine Triphosphate / Q000032:analysis; D000681:Amylases / Q000097:blood; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology* / Q000627:therapeutic use; D015415:Biomarkers; D003907:Dexamethasone / Q000494:pharmacology* / Q000627:therapeutic use; D006854:Hydrocortisone / Q000494:pharmacology* / Q000627:therapeutic use; D015850:Interleukin-6 / Q000097:blood; D008099:Liver / Q000378:metabolism / Q000473:pathology; D008168:Lung / Q000378:metabolism / Q000473:pathology; D008297:Male; D015735:Mifepristone / Q000494:pharmacology*; D009102:Multiple Organ Failure / Q000209:etiology / Q000503:physiopathology; D009504:Neutrophils / Q000201:enzymology; D010179:Pancreas / Q000378:metabolism / Q000473:pathology; D010195:Pancreatitis / Q000139:chemically induced / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D009195:Peroxidase / Q000032:analysis; D011292:Premedication; D051381:Rats; D017208:Rats, Wistar; D013656:Taurocholic Acid / Q000633:toxicity
chemical_list: D000893:Anti-Inflammatory Agents; D015415:Biomarkers; D015850:Interleukin-6; D015735:Mifepristone; D013656:Taurocholic Acid; D003907:Dexamethasone; D000255:Adenosine Triphosphate; D009195:Peroxidase; D000681:Amylases; D006854:Hydrocortisone