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 language||English (US)|
|Journal||American Journal of Physiology|
|Issue number||3 PART 1|
|State||Published - 1997|
- Heme oxygenase
ASJC Scopus subject areas
- Physiology (medical)