An Oral Adsorbent Downregulates Renal Expression of Genes That Promote Interstitial Inflammation and Fibrosis in Diabetic Rats
書誌事項
- 公開日
- 2002
- 権利情報
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- https://www.karger.com/Services/SiteLicenses
- https://www.karger.com/Services/SiteLicenses
- DOI
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- 10.1159/000064108
- 公開者
- S. Karger AG
この論文をさがす
説明
<jats:p>Background/Aims: An oral adsorbent, AST-120, removes uremic toxins such as indoxyl sulfate, and delays the progression of renal failure. This study was designed to investigate the effects of AST-120 on the molecular basis of interstitial inflammation and fibrosis, using Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a model of non-insulin-dependent diabetes mellitus. Methods: Four weeks after unilateral nephrectomy, the uninephrectomized OLETF (1/2NxOLETF) rats were divided into two groups: AST-120-administered and control 1/2NxOLETF rats. After the administration of AST-120 for 48 weeks, we examined the effects of AST-120 on renal functional, pathological, and gene expressional changes. Results: The administration of AST-120 to the 1/2NxOLETF rats attenuated the progression of renal dysfunction, proteinuria, glomerular sclerosis, tubular injury, and interstitial inflammation and fibrosis. AST-120 significantly reduced renal expression of intercellular adhesion molecule (ICAM)-1, osteopontin, monocyte chemotactic protein (MCP)-1, and transforming growth factor (TGF)-β1, as well as clusterin. All the five molecules were expressed mainly in tubular cells. AST-120 also decreased serum and urinary levels of indoxyl sulfate and the overload of indoxyl sulfate in tubular cells. Conclusion: AST-120 ameliorates tubulointerstitial injury by reducing renal expression of ICAM-1, osteopontin, MCP-1, TGF-β1 and clusterin in 1/2NxOLETF rats.</jats:p>
収録刊行物
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- Nephron
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Nephron 92 (3), 635-651, 2002
S. Karger AG