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This Article Full Text Full Text (PDF) All Versions of this Article: 296/5/F1146    most recent 90732.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Ghosh, S. S. Articles by Gehr, T. W. B. Search for Related Content PubMed PubMed Citation Articles by Ghosh, S. S. Articles by Gehr, T. W. B.

Curcumin ameliorates renal failure in 5/6 nephrectomized rats: role of inflammation

Divisions of ¹Nephrology, ²Pathology, and ³Anatomy, Virginia Commonwealth University Medical Center, and ⁴Division of Pulmonary Medicine, Virginia Commonwealth University, Richmond, Virginia

Submitted 8 December 2008 ; accepted in final form 10 February 2009

TNF- and NF-B play important roles in the development of inflammation in chronic renal failure (CRF). In hepatic cells, curcumin is shown to antagonize TNF--elicited NF-B activation. In this study, we hypothesized that if inflammation plays a key role in renal failure then curcumin should be effective in improving CRF. The effectiveness of curcumin was compared with enalapril, a compound known to ameliorate human and experimental CRF. Investigation was conducted in Sprague-Dawley rats where CRF was induced by 5/6 nephrectomy (Nx). The Nx animals were divided into untreated (Nx), curcumin-treated (curcumin), and enalapril-treated (enalapril) groups. Sham-operated animals served as a control. Renal dysfunction in the Nx group, as evidenced by elevated blood urea nitrogen, plasma creatinine, proteinuria, segmental sclerosis, and tubular dilatation, was significantly reduced by curcumin and enalapril treatment. However, only enalapril significantly improved blood pressure. Compared with the control, the Nx animals had significantly higher plasma and kidney TNF-, which was associated with NF-B activation and macrophage infiltration in the kidney. These changes were effectively antagonized by curcumin and enalapril treatment. The decline in the anti-inflammatory peroxisome proliferator-activated receptor (PPAR) seen in Nx animals was also counteracted by curcumin and enalapril. Studies in mesangial cells were carried out to further establish that the anti-inflammatory effect of curcumin in vivo was mediated essentially by antagonizing TNF-. Curcumin dose dependently antagonized the TNF--mediated decrease in PPAR and blocked transactivation of NF-B and repression of PPAR, indicating that the anti-inflamatory property of curcumin may be responsible for alleviating CRF in Nx animals.

TNF-; remnant; angiotensin; PPAR