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.

C F Nathan (1987)

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

Kazuhide Okuda, M. Sporn, W Border … (1990)

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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Urinary 8-hydroxy-2'-deoxyguanosine as a biological marker of in vivo oxidative DNA damage.

Eduardo Gimeno, James Ames, Mark Shigenaga (1989)

DNA is subject to constant oxidative damage from endogenous oxidants. The oxidized DNA is continuously repaired and the oxidized bases are excreted in the urine. A simple routine analytical procedure is described for urinary 8-hydroxy-2'-deoxyguanosine, an oxidative DNA damage adduct, as an indicator of oxidative damage in humans and rodents. This adduct was purified from human urine and characterized. The described assay employs a series of solid-phase extraction steps that separate 8-hydroxy-2'-deoxyguanosine from other urinary constituents, followed by analysis by gradient reversed-phase HPLC coupled to a dual-electrode high-efficiency electrochemical detection system. Analysis of urine from three species by this method indicates that mice excrete approximately 3.3-fold more 8-hydroxy-2'-deoxyguanosine than humans (582 vs. 178 residues per cell per day), a result that supports the proposal that oxidative damage to DNA increases in proportion to species-specific basal metabolic rates.

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Author and article information

Journal

Journal ID (publisher-id): KBR

Journal ID (nlm-ta): Kidney Blood Press Res

Journal ID (doi): 10.1159/issn.1420-4096

Title: Kidney and Blood Pressure Research

Publisher: S. Karger AG

ISSN (Print): 1420-4096

ISSN (Electronic): 1423-0143

Publication date Subscription-year: 2007

Publication date (Print): July 2007

Publication date (Electronic): 18 June 2007

Volume: 30

Issue: 4

Pages: 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

Publisher ID: 104090 Other ID: Kidney Blood Press Res 2007;30:212–223

DOI: 10.1159/000104090

PubMed ID: 17587863

SO-VID: 8a3fa13d-46fa-45d5-b9f9-d2ba5bc58355

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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.

History

Date received : 25 January 2007

Date accepted : 22 April 2007

Page count

Figures: 12, Tables: 1, References: 50, Pages: 12

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Renoprotective Effects of Rosiglitazone in Stroke-Prone Spontaneously Hypertensive Rats

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Abstract

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Karger: Nephrology

Most cited references 30

Secretory products of macrophages.

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

Urinary 8-hydroxy-2'-deoxyguanosine as a biological marker of in vivo oxidative DNA damage.

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