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12,14-prostaglandin J2 on bleomycin-induced lung injury
1 Dept of Clinical and Experimental Medicine and Pharmacology, Torre Biologica, Policlinico Universitario, Messina, and 2 Dept of Internal and Specialist Medicine, Section of Respiratory Diseases and Infectious Diseases, and 3 Dept of Pharmaceutical Sciences, University of Catania, Catania, Italy. 4 Dept of Experimental Medicine & Nephrology, The William Harvey Research Institute, St. Bartholomew's and The Royal London School of Medicine and Dentistry, London, UK. 5 Authors contributed equally to the study.
CORRESPONDENCE: S. Cuzzocrea, Dept of Clinical and Experimental Medicine and Pharmacology, School of Medicine, University of Messina, Torre Biologica, Policlinico Universitario, Via C. Valeria, Gazzi, 98100 Messina, Italy. Fax: 39 0902213300. E-mail: salvator@unime.it
Keywords: Bleomycin, 15-deoxy-
12,14-prostaglandin J2, lung injury, peroxisome proliferator-activated receptor-
, rosiglitazone
Received: April 27, 2004
Accepted September 14, 2004
Thiazolidinedione rosiglitazone and 15-deoxy-
Mice subjected to intratracheal administration of bleomycin developed significant lung injury. An increase in immunoreactivity to nitrotyrosine, poly(ADP ribose) polymerase (PARP) and inducible nitric oxide synthase as well as a significant loss of body weight and mortality was observed in the lung of bleomycin-treated mice.
Administration of the two PPAR-
These results demonstrate that the two peroxisome proliferator-activated receptor-
12,14-prostaglandin J2 (15d-PGJ2), are two peroxisome proliferator-activated receptor (PPAR)- ligands. The aim of this study was to investigate the effect of rosiglitazone and 15d-PGJ2 on the lung injury caused by bleomycin administration. agonists rosiglitazone (10 mg·kg–1 i.p.) and 15d-PGJ2 (30 µg·kg–1 i.p.) significantly reduced the: 1) loss of body weight, 2) mortality rate, 3) infiltration of the lung with polymorphonuclear neutrophils (myeloperoxidase activity), 4) oedema formation, and 5) histological evidence of lung injury. Administration of rosiglitazone and 15d-PGJ2 also markedly reduced the nitrotyrosine, PARP and inducible nitric oxide synthase formation. In addition, treatment with the PPAR- antagonist bisphenol A diglycidyl ether (1 mg·kg–1 i.p. 30 min before the rosiglitazone or 15d-PGJ2) significantly antagonised the effect of the two PPAR- agonists. agonists, rosiglitazone and 15-deoxy-12,14-prostaglandin J2, significantly reduce lung injury induced by bleomycin in mice.
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