Journal
AMERICAN JOURNAL OF NEPHROLOGY
Volume 31, Issue 6, Pages 527-533Publisher
KARGER
DOI: 10.1159/000309756
Keywords
Annexin A1; Tacrolimus; Immunosuppression
Categories
Funding
- Conselho Nacional de Desenvolvimento Cientfico e Tecnologico - CNPq [306074/2007-9, 307371/2006-9]
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo [2008/01048-9]
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Background: Tacrolimus (FK) is currently widely used in transplant immunosuppression and the treatment of autoimmune diseases. However, FK induces nephrotoxicity which is characterized by functional and structural renal injury. The ubiquitous protein annexin A1 (ANXA1) has potent anti-inflammatory effects and protects against ischemia/reperfusion injury. We investigated the effects of exogenous ANXA1 treatment in an experimental model of acute FK nephrotoxicity. Methods: Munich-Wistar rats received a low-salt diet for 1 week and were randomized to treatment with ANXA1 (Ac2-26 peptide 0.5 mg/kg/day s.c.), FK (6 mg/kg/day p.o.), association (FK+ANXA1) and vehicles (1 ml/kg/day) for 7 days. Results: FK induced a significant decrease in glomerular filtration rate and renal blood flow, and a significant increase in renal vascular resistance. In addition, FK caused extensive acute tubule-interstitial damage and an increase in anti-inflammatory ANXA1 expression in renal tissue. Exogenous ANXA1 treatment reduced FK-induced tubular dilatation and macrophage infiltration. For the first time, we observed that FK augmented ANXA1 expression in renal tissue. Conclusion: Exogenous ANXA1 treatment partially protected against FK-induced tubular injury and macrophage infiltration, and may be targeted in renal intervention strategies. Copyright (C) 2010 S. Karger AG, Basel
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