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      Nitrooleic Acid Protects against Cisplatin Nephropathy: Role of COX-2/mPGES-1/PGE 2 Cascade

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          Abstract

          Nitrooleic acid (OA-NO 2) is an endogenous lipid product which has novel signaling properties, particularly the activation of peroxisome proliferator-activated receptors. The current study aimed to evaluate the protective effects of OA-NO 2 against cisplatin-induced kidney injury in mice. Mice were pretreated with OA-NO 2 for 48 h before cisplatin administration, and the cisplatin-caused nephrotoxicity was evaluated. After the cisplatin treatment (72 h), the vehicle-treated mice displayed renal dysfunction, as evidenced by the elevated plasma urea and creatinine, which was consistent with the histological damage, such as tubular necrosis, dilation, protein cast, and desquamation of epithelial cells. In contrast, the severity of the renal dysfunction and histological change were reduced in the OA-NO 2 pretreated mice. The renal COX-2 and mPGES-1 mRNAs and their respective proteins expression, together with the renal PGE 2 amounts, were induced by the cisplatin treatment, but their initiation was reduced by OA-NO 2. Moreover, the circulating TNF- α, renal TNF- α, IL-1 β, MCP-1, ICAM-1, and VACAM-1 mRNA levels were higher in the cisplatin-treated mice, compared with the controls, but they were attenuated in the OA-NO 2 pretreatment group. In summary, the pretreatment with OA-NO 2 remarkably ameliorated the cisplatin-induced kidney injury in mice, possibly via the inhibition of the inflammatory response, associated with the COX-2/mPGES-1/PGE 2 cascade.

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          Most cited references31

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          TNF-α mediates chemokine and cytokine expression and renal injury in cisplatin nephrotoxicity

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            Impaired inflammatory and pain responses in mice lacking an inducible prostaglandin E synthase.

            Prostaglandin (PG)E2 is a potent mediator of pain and inflammation, and high levels of this lipid mediator are observed in numerous disease states. The inhibition of PGE2 production to control pain and to treat diseases such as rheumatoid arthritis to date has depended on nonsteroidal antiinflammatory agents such as aspirin. However, these agents inhibit the synthesis of all prostanoids. To produce biologically active PGE2, PGE synthases catalyze the isomerization of PGH2 into PGE2. Recently, several PGE synthases have been identified and cloned, but their role in inflammation is not clear. To study the physiological role of the individual PGE synthases, we have generated by targeted homologous recombination a mouse line deficient in microsomal PGE synthase 1 (mPGES1) on the inbred DBA/1lacJ background. mPGES1-deficient (mPGES1-/-) mice are viable and fertile and develop normally compared with wild-type controls. However, mPGES1-/- mice displayed a marked reduction in inflammatory responses compared with mPGES1+/+ mice in multiple assays. Here, we identify mPGES1 as the PGE synthase that contributes to the pathogenesis of collagen-induced arthritis, a disease model of human rheumatoid arthritis. We also show that mPGES1 is responsible for the production of PGE2 that mediates acute pain during an inflammatory response. These findings suggest that mPGES1 provides a target for the treatment of inflammatory diseases and pain associated with inflammatory states.
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              The Natural History of the Systemic Inflammatory Response Syndrome (SIRS)

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                Author and article information

                Journal
                Mediators Inflamm
                Mediators Inflamm
                MI
                Mediators of Inflammation
                Hindawi Publishing Corporation
                0962-9351
                1466-1861
                2015
                11 March 2015
                : 2015
                : 293474
                Affiliations
                1Department of Nephrology, Provincial Hospital Affiliated to Shandong University, No. 324 Jingwu Road, Jinan, Shandong 250013, China
                2Department of Internal Medicine, University of Utah and Salt Lake Veterans Affairs Medical Center, Salt Lake City, UT 84112, USA
                Author notes

                Academic Editor: Alex Kleinjan

                Article
                10.1155/2015/293474
                4377489
                92e4c666-5e45-4a53-86ba-df34beed8e1d
                Copyright © 2015 Haiping Wang 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.

                History
                : 19 September 2014
                : 16 January 2015
                : 21 January 2015
                Categories
                Research Article

                Immunology
                Immunology

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