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GASTROINTESTINAL, HEPATIC, PULMONARY, AND RENAL

Peroxisome Proliferator-Activated Receptor- Contributes to the Resolution of Inflammation after Renal Ischemia/Reperfusion Injury

Centre for Translational Medicine and Therapeutics, William Harvey Research Institute, St. Bartholomew's and the Royal London School of Medicine and Dentistry, Queen Mary-University of London, United Kingdom (N.S.A.P., C.T.); Department of Clinical and Experimental Medicine and Pharmacology, Institute of Pharmacology, University of Messina, Messina, Italy and IRCCS Centro Neurolesi "Bonino-Pulejo," Messina, Italy (R.d.P., E.M., S.C.); and Department of Veterinary and Agricultural Science, University of Teramo, Teramo, Italy (D.B.)

This study was designed to elucidate the role of peroxisome proliferator-activated receptor (PPAR)- in the development of inflammation after ischemia/reperfusion injury of the kidney. We have evaluated the effects of ischemia/reperfusion on renal dysfunction, injury, and inflammation in wild-type mice or mice in which the gene for PPAR- has been deleted [PPAR-(-/-)] and then treated with the PPAR- agonist fenofibrate. Mice were subjected to bilateral renal ischemia (30 min) and reperfusion (24 h) and received fenofibrate (3 mg/kg i.p.) before reperfusion. Plasma creatinine, urea, and aspartate aminotransferase were all used as indicators of renal dysfunction and injury. Kidneys were used for histological and immunohistochemical analysis and markers of inflammation. Fenofibrate significantly attenuated the degree of renal dysfunction, injury, and inflammation caused by ischemia/reperfusion injury. The degree of renal dysfunction, injury, and inflammation caused by ischemia/reperfusion was also significantly augmented in PPAR-(-/-) mice compared with their wild-type littermates. It is interesting that fenofibrate did not protect PPAR-(-/-) mice against ischemia/reperfusion injury. Therefore, we propose that ligands of PPAR- may be useful in the treatment of renal ischemia/reperfusion injury and that endogenous PPAR- limits the degree of renal dysfunction, injury, and inflammation associated with ischemia/reperfusion injury.

Address correspondence to: Dr. Nimesh S. A. Patel, Centre for Translational Medicine and Nephrology, William Harvey Research Institute, St. Bartholomew's and The Royal London School of Medicine and Dentistry, Queen Mary-University of London, Charterhouse Square, London EC1M 6BQ, United Kingdom. E-mail: n.s.patel{at}qmul.ac.uk

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				H.-H. Chen, T.-W. Chen, and H. Lin Prostacyclin-induced peroxisome proliferator-activated receptor-{alpha} translocation attenuates NF-{kappa}B and TNF-{alpha} activation after renal ischemia-reperfusion injury Am J Physiol Renal Physiol, October 1, 2009; 297(4): F1109 - F1118. [Abstract] [Full Text] [PDF]