Expression of oxidative stress-responsive genes and cytokine genes during caerulein-induced acute pancreatitis

Kai Fu, Michael P. Sarras, Robert C. De Lisle, Glen K. Andrews

Research output: Contribution to journalArticlepeer-review

9 Scopus citations


Oxidative stress and the inflammatory response may play roles in the pathogenesis of acute pancreatitis. Herein, we characterized pancreatic expression of oxidative stress-responsive genes [c-fos, heme oxygenase-1 (HO-1), and metallothionein-I (MT-I)] and cytokine genes [interleukin-lβ (IL-lβ ), IL-6, and tumor necrosis factorα (TNFα )] during caerulein-induced acute pancreatitis in the mouse, c-fos, HO-1, and MT-I mRNAs were coordinately and rapidly (3-7 h) upregulated, and HO-1 and MT-I protein levels were increased slightly in the pancreas during acute pancreatitis. In addition, IL-lβ , IL-6, and TNFα mRNAs were rapidly (7 h) upregulated in the pancreas, and intrapancreatic IL-lβ and IL-6 protein levels rapidly increased (3-fold and 6.4-fold, respectively) during acute pancreatitis. These studies suggest that oxidative stress and inflammation each occur in the pancreas during the early stages of acute pancreatitis. However, under a limited set of experimental conditions, we found that an insult that causes pancreatic oxidative stress (diethylmaleate) or one that induces an inflammatory response (bacterial lipopolysaccharide), or a combination of these agents, did not cause the changes characteristic of acute pancreatitis. Therefore, simply inducing oxidative stress and/or inflammation may be insufficient to initiate acute pancreatitis.

Original languageEnglish (US)
Pages (from-to)G647-G654
JournalAmerican Journal of Physiology
Issue number3 PART 1
StatePublished - 1997


  • C-fos
  • Glutathione
  • Heme oxygenase
  • Inflammation
  • Interleukin
  • Metallothionein
  • Mouse

ASJC Scopus subject areas

  • Physiology (medical)


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