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Role of peroxisome proliferator-activated receptor γ activation in gastric mucosal ulcer healing

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image of Inflammopharmacology

Peroxisome proliferator-activated receptor-γ (PPARγ) is a ligand-dependent transcription factor, belonging to the steroid hormone receptor family, known to play a pivotal role in the resolution of inflammation. In this study, we investigated the effect of a specific PPARγ ligand, ciglitazone, on the course of gastric ulcer healing by analyzing apoptotic processes and the mucosal activity of inducible nitric oxide synthase (NOS-2), and the expression cyclooxygenases (COX-1 and COX-2) responsible for prostaglandin (PG) generation. Groups of rats with experimentally induced gastric mucosal ulcers were administered twice daily for up to14 days with ciglitazone at 5, 10, and 15 mg/kg or the vehicle, and their mucosal tissue subjected to assessment of ulcer healing rate and biochemical measurements. The ulcer onset, characterized by a massive epithelial apoptosis and up-regulation of NOS-2 and COX-2 protein expression, was reflected in a marked increase in the mucosal PGE2 generation and NOS-2 activity, whereas healing was accompanied by a decrease in apoptosis, drop in PGE2 and NOS-2 activity, and a decrease in COX-2 and NOS-2 protein expression. The mucosal expression of COX-1 protein, however, remained unchanged. Administration of ciglitazone led to a significant dose-dependent acceleration in the mucosal reduction of PGE2 generation, epithelial cell apoptosis and NOS-2 activity, and produced a marked decline in COX-2 and NOS-2 protein expression, but the rate of ulcer healing remained unaffected. Our findings with PPARγ activator, ciglitazone, thus provide evidence that the products of induced expression of NOS-2 and COX-2 enzymes, associated with the ulcer onset, do not play a significant role in gastric ulcer healing, but rather reflect a general pattern of mucosal inflammatory responses to injury.


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