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Mediators of Inflammation
Volume 2015, Article ID 693260, 12 pages
http://dx.doi.org/10.1155/2015/693260
Research Article

Genetic Deletion of Soluble Epoxide Hydrolase Attenuates Inflammation and Fibrosis in Experimental Obstructive Nephropathy

1Department of Physiology, National Yang-Ming University, Taipei 11221, Taiwan
2Institute of Anatomy and Cell Biology, National Yang-Ming University, Taipei 11221, Taiwan
3Division of Nephrology, Department of Medicine and Immunology Research Centre, Taipei Veterans General Hospital, Taipei 11221, Taiwan
4Division of Nephrology, Buddhist Tzu Chi General Hospital, Taipei Branch, Taipei 23142, Taiwan
5Department of Nursing, Chang Gung Institute of Technology, Taoyuan 33303, Taiwan

Received 29 September 2014; Revised 28 November 2014; Accepted 7 December 2014

Academic Editor: Tânia Silvia Fröde

Copyright © 2015 Chin-Wei Chiang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Soluble epoxide hydrolase (sEH) is abundantly expressed in kidney and plays a potent role in regulating inflammatory response in inflammatory diseases. However, the role of sEH in progression of chronic kidney diseases such as obstructive nephropathy is still elusive. In current study, wild-type (WT) and sEH deficient (sEH−/−) mice were subjected to the unilateral ureteral obstruction (UUO) surgery and the kidney injury was evaluated by histological examination, western blotting, and ELISA. The protein level of sEH in kidney was increased in UUO-treated mice group compared to nonobstructed group. Additionally, UUO-induced hydronephrosis, renal tubular injury, inflammation, and fibrosis were ameliorated in sEH−/− mice with the exception of glomerulosclerosis. Moreover, sEH−/− mice with UUO showed lower levels of inflammation-related and fibrosis-related protein such as monocyte chemoattractant protein-1, macrophage inflammatory protein-2, interleukin-1β (IL-1β), IL-6, inducible nitric oxide synthase, collagen 1A1, and α-actin. The levels of superoxide anion radical and hydrogen peroxide as well as NADPH oxidase activity were also decreased in UUO kidneys of sEH−/− mice compared to that observed in WT mice. Collectively, our findings suggest that sEH plays an important role in the pathogenesis of experimental obstructive nephropathy and may be a therapeutic target for the treatment of obstructive nephropathy-related diseases.