Skip to content


Open Access

Differential anti-inflammatory properties of peroxisome proliferator-activated receptors (PPAR) α and γ in experimental pancreatitis

  • Thomas Griesbacher1Email author,
  • Veronika Pommer1,
  • Rufina Schuligoi1 and
  • Bernhard A Peskar1
BMC Pharmacology20077(Suppl 2):A20

Published: 14 November 2007


PancreatitisAcute PancreatitisRosiglitazoneCholecystokininClofibrate

Perfluorooctanoic acid (PFOA) has anti-inflammatory effects in models of cutaneous inflammation, possibly via activation of PPAR-α and PPAR-γ. We have therefore investigated whether PFOA has similar effects in a model of acute oedematous pancreatitis and whether such effects could be explained by agonism at PPAR-α or PPAR-γ. Acute pancreatitis was induced in anesthetized rats by i.v. infusion of the cholecystokinin analogue, caerulein. The PPAR-α agonist clofibrate or the PPAR-γ agonist rosiglitazone were injected s.c. before the experiments. Pancreatic oedema, neutrophil activation and production of prostaglandin (PG) E2 and prostacyclin (via 6-keto-PGF) were assessed in the pancreas. Acute pancreatitis caused significant oedema formation, neutrophil activation as assessed by myeloperoxidase activity in the tissue, and increased synthesis of pro-inflammatory prostanoids. Neutrophil activation was unaffected by clofibrate but was abolished by rosiglitazone. In contrast, prostanoid synthesis was unaffected by rosiglitazone but was inhibited by clofibrate. In conclusion, our data demonstrate that activation of PPAR-α and PPAR-γ has differential anti-inflammatory effects in acute interstitial-oedematous pancreatitis. Neutrophil activation is sensitive to inhibition by PPAR-γ activation while the production of pro-inflammatory prostanoids can be attenuated by activation of PPAR-α. Thus, the anti-inflammatory potential of PPAR-α and PPAR-γ ligands should be further investigated.

Authors’ Affiliations

Institute of Experimental and Clinical Pharmacology, Medical University of Graz, Austria


© Griesbacher et al; licensee BioMed Central Ltd. 2007

This article is published under license to BioMed Central Ltd.