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      Protective effects of relaxin against cisplatin-induced nephrotoxicity in rats.

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          Abstract

          Cisplatin (CDDP)-induced acute kidney injury (AKI) involves pro-inflammatory responses, apoptosis of renal tubular epithelial cells and vascular damage. AKI increases the risk of chronic kidney disease. Relaxin (RLX) has anti-apoptotic and anti-fibrosis properties. The aim of this study was to investigate the effects of RLX on CDDP-induced nephrotoxicity.

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          Cisplatin-induced acute renal failure is associated with an increase in the cytokines interleukin (IL)-1beta, IL-18, IL-6, and neutrophil infiltration in the kidney.

          Sarah Faubel, Eli Lewis, Leonid Reznikov … (2007)
          We have demonstrated that caspase-1-deficient (caspase-1(-/-)) mice are functionally and histologically protected against cisplatin-induced acute renal failure (ARF). Caspase-1 exerts proinflammatory effects via the cytokines interleukin (IL)-1beta, IL-18, IL-6, and neutrophil recruitment. We sought to determine the role of the cytokines IL-1beta, IL-18, and IL-6 and neutrophil recruitment in cisplatin-induced ARF. We first examined IL-1beta; renal IL-1beta increased nearly 2-fold in cisplatin-induced ARF and was reduced in the caspase-1(-/-) mice. However, inhibition with IL-1 receptor antagonist (IL-1Ra) did not attenuate cisplatin-induced ARF. Renal IL-18 increased 2.5-fold; however, methods to inhibit IL-18 using IL-18 antiserum and transgenic mice that overproduce IL-18-binding protein (a natural inhibitor of IL-18) did not protect. Renal IL-6 increased 3-fold; however, IL-6-deficient (IL-6(-/-)) mice still developed cisplatin-induced ARF. We next examined neutrophils; blood neutrophils increased dramatically after cisplatin injection; however, prevention of peripheral neutrophilia and renal neutrophil infiltration with the neutrophil-depleting antibody RB6-8C5 did not protect against cisplatin-induced ARF. In summary, our data demonstrated that cisplatin-induced ARF is associated with increases in the cytokines IL-1beta, IL-18, and IL-6 and neutrophil infiltration in the kidney. However, inhibition of IL-1beta, IL-18, and IL-6 or neutrophil infiltration in the kidney is not sufficient to prevent cisplatin-induced ARF.
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            Platinum nephrotoxicity.

            Nicolaos Madias, John Harrington (1978)
            Platinum coordination complexes have recently been introduced in cancer chemotherapy with considerable success. However, significant nephrotoxicity has emerged as a factor that limits the therapeutic usefulness of these compounds. In this article we review the available knowledge on platinum nephrotoxicity and its prevention that has been derived from both toxicologic studies in animals and clinical trials in human subjects.
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              Regulation and pathological role of p53 in cisplatin nephrotoxicity.

              Man Jiang, Zheng Dong (2008)
              Cisplatin is one of the most potent chemotherapy drugs widely used for cancer treatment. However, its use is limited by side effects in normal tissues, particularly the kidneys. Recent studies, using both in vitro and in vivo experimental models, have suggested a critical role for p53 in cisplatin nephrotoxicity. The signaling pathways upstream and downstream of p53 are being investigated and related to renal cell injury and death. Along with the mechanistic studies, renoprotective approaches targeting p53 have been suggested. Further research may integrate p53 signaling with other nephrotoxic signaling pathways, providing a comprehensive understanding of cisplatin nephrotoxicity and leading to the development of effective renoprotective strategies during cancer therapy.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Nephron Exp. Nephrol.
                Title: Nephron. Experimental nephrology
                Publisher: S. Karger AG
                ISSN (Electronic): 1660-2129
                ISSN (Print): 1660-2129
                Publication date (Electronic): 2014
                Volume: 128
                Issue: 1-2
                Affiliations
                [1 ] Department of Clinical Nutrition, School of Food and Nutritional Sciences, University of Shizuoka, Shizuoka, Japan.
                Article
                Publisher Item ID: 000365852
                DOI: 10.1159/000365852
                PubMed ID: 25403022
                SO-VID: 61373f72-760f-46a6-b90f-df80c6873c9b
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