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      Renoprotective Effects of Rosiglitazone in Stroke-Prone Spontaneously Hypertensive Rats

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          Abstract

          Background/Aims: Rosiglitazone (RGTZ) has a protective effect against various types of injury. We evaluated the effects of RGTZ on renal injury in a stroke-prone spontaneously hypertensive rat (SHRSP) model. Methods: Male SHRSP rats were observed with or without RGTZ treatment for 10 weeks. Age-matched male Wistar-Kyoto rats were used as controls. The effect of RGTZ on hypertensive nephropathy was evaluated by assessing renal function, pathology, pro-inflammatory cytokine (osteopontin), profibrotic cytokine (βig-h3), apoptotic cell death (TUNEL staining and caspase 3 expression), marker of oxidative stress (8-OHdG) and endothelial damage (eNOS). Results: RGTZ treatment improved renal function and histopathology compared with SHRSP rats without treatment (p < 0.05). Osteopontin and βig-h3 were significantly increased in SHRSP rat kidneys, but RGTZ treatment decreased both mediators. Apoptotic cell death was increased in renal tubular cells in the injured area in SHRSP rat kidneys, but RGTZ treatment decreased apoptotic cell death and caspase 3 expression. Increased urinary 8-OHdG excretion and decreased eNOS in SHRSP rats was reversed with RGTZ treatment. Conclusions: RGTZ protects hypertensive nephropathy in SHRSP rats.

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          Most cited references 30

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          Secretory products of macrophages.

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            Suppression of experimental glomerulonephritis by antiserum against transforming growth factor beta 1.

            Glomerulonephritis is an inflammation of the kidney characterized by the accumulation of extracellular matrix within the damaged glomeruli, impaired filtration and proteinuria. In its progressive form, the disease destroys kidney function leading to uraemia and death, unless dialysis therapy or kidney transplantation is available. The pathogenesis of glomerulonephritis is incompletely understood, but the eliciting factor is thought often to be an immunological injury to mesangial and/or other resident cells in the glomeruli. We have used an animal model of acute mesangial proliferative glomerulonephritis to show that this disease is associated with increased production and activity of transforming growth factor beta 1 (TGF-beta 1), an inducer of extracellular matrix production. Here we report that administration of anti-TGF-beta 1 at the time of induction of the glomerular disease suppresses the increased production of extracellular matrix and dramatically attenuates histological manifestations of the disease. These results provide direct evidence for a causal role of TGF-beta 1 in the pathogenesis of the experimental disease and suggest a new approach to the therapy of glomerulonephritis.
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              Essential hypertension: renin and aldosterone, heart attack and stroke.

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                Author and article information

                Journal
                KBR
                Kidney Blood Press Res
                10.1159/issn.1420-4096
                Kidney and Blood Pressure Research
                S. Karger AG
                1420-4096
                1423-0143
                2007
                July 2007
                18 June 2007
                : 30
                : 4
                : 212-223
                Affiliations
                Cell Death Research Center, Division of Nephrology, Kangnam St. Mary’s Hospital, Catholic University of Korea, Seoul, Korea; Department of Internal Medicine, The Affiliated Hospital, Yanbian University Medical College, Yanji City, Jilin, PR China
                Article
                104090 Kidney Blood Press Res 2007;30:212–223
                10.1159/000104090
                17587863
                © 2007 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 12, Tables: 1, References: 50, Pages: 12
                Categories
                Original Paper

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