The role of inflammatory mediators in severe acute pancreatitis and regulation of glucocorticoids

  • Zi Fa Wang
  • , Cheng En Pan
  • , Yi Lu
  • , Shab Gao Liu
  • , Guan Jun Zhang
  • , Xue Bin Zhang

Research output: Contribution to journalArticlepeer-review

28 Scopus citations

Abstract

Objective: To investigate the effect of glucocorticoids on systemic inflammatory mediator release in rats with acute pancreatitis and the outcome of dexamethasone in treatment of acute pancreatitis. Methods: Sixty-eight Wistar rats were divided into sham, acute pancreatitis, and treatment (intravenous dexamethasone 0.5 mg/kg) groups. Experimental acute pancreatitis was induced by the injection of 5% sodium taurocholate (0.1 ml/100 mg body weight) into the pancreatic-biliary duct. The blood samples were obtained and examined for 6-keto-PGI1α, TXB2 and IL-6 postoperatively at 3, 6 and 12 hours, respectively. The pancreatic samples were evaluated by a blinded method. Twelve-hour survival rate was determined and compared between the groups. Results: The high serum concentrations of 6-keto-PGI1α, TXB2 and IL-6 were noted in the rats with acute pancreatitis associated with pancreatic hemorrhage and necrosis. Their 12-hour survival rate was 42.9%. The rats in the treatment group survived with significantly reduced serum concentrations of 6-keto-PGI1α, TXB2 and IL-6 (P < 0.05 . Their pancreatic morphology was normal. Conclusion: Dexamethasone may reduce the serum concentration of 6-keto-PGI1α, TXB2, and IL-6, and the severity of acute pancreatitis while increasing the survival rate of rats with acute pancreatitis.

Original languageEnglish
Pages (from-to)458-462
Number of pages5
JournalHepatobiliary and Pancreatic Diseases International
Volume2
Issue number3
StatePublished - Aug 2003

Keywords

  • Acute pancreatitis
  • Dexamethasone
  • Inflammatory mediators

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