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      Renoprotective Effects of Rosiglitazone in Stroke-Prone Spontaneously Hypertensive Rats

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          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.


                Author and article information

                Kidney Blood Press Res
                Kidney and Blood Pressure Research
                S. Karger AG
                July 2007
                18 June 2007
                : 30
                : 4
                : 212-223
                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
                104090 Kidney Blood Press Res 2007;30:212–223
                © 2007 S. Karger AG, Basel

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


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