Annexin A1 protein attenuates cyclosporine-induced renal hemodynamics changes and macrophage infiltration in rats

Annexin A1 protein attenuates cyclosporine-induced renal hemodynamics changes and macrophage infiltration in rats

Autor Araujo, Leandro Pires Autor UNIFESP Google Scholar
Truzzi, Renata Ramos Google Scholar
Florido Mendes, Gloria Elisa Google Scholar
Mendes Luz, Marcus Alexandre Google Scholar
Burdmann, Emmanuel A. Google Scholar
Oliani, Sonia Maria Autor UNIFESP Google Scholar
Instituição São Paulo State Univ UNESP
Universidade Federal de São Paulo (UNIFESP)
Sao Jose do Rio Preto Med Sch
Universidade de São Paulo (USP)
Resumo Cyclosporine (CsA) remains an important immunosuppressant for transplantation and for treatment of autoimmune diseases. the most troublesome side effect of CsA is renal injury. Acute CsA-induced nephrotoxicity is characterized by reduced renal blood flow (RBF) and glomerular filtration rate (GFR) due to afferent arteriole vasoconstriction. Annexin A1 (ANXA1) is a potent anti-inflammatory protein with protective effect in renal ischemia/reperfusion injury. Here we study the effects of ANXA1 treatment in an experimental model of acute CsA nephrotoxicity.Salt-depleted rats were randomized to treatment with VH (vehicles 1 mL/kg body weight/day), ANXA1 (Ac2-26 peptide 1 mg/kg body weight/day intraperitoneally), CsA (20 mg/kg body weight/day subcutaneously) and CsA + ANXA1 (combination) for seven days. We compared renal function and hemodynamics, renal histopathology, renal tissue macrophage infiltration and renal ANXA1 expression between the four groups.CsA significantly impaired GFR and RBF, caused tubular dilation and macrophage infiltration and increased ANXA1 renal tissue expression. Treatment with ANXA1 attenuated CSA-induced hemodynamic changes, tubular injury and macrophage infiltration.ANXA1 treatment attenuated renal hemodynamic injury and inflammation in an acute CsA nephrotoxicity model.
Assunto Acute renal injury
Annexin A1
Cyclosporine nephrotoxicity
Immunosuppression
Inflammation
Idioma Inglês
Financiador Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Número do financiamento FAPESP: 2008/01,048-9
CNPq: 306,074/2007-9
CNPq: 307,371/2006-9
Data 2012-03-01
Publicado em Inflammation Research. Basel: Springer Basel Ag, v. 61, n. 3, p. 189-196, 2012.
ISSN 1023-3830 (Sherpa/Romeo, fator de impacto)
Editor Springer
Extensão 189-196
Fonte http://dx.doi.org/10.1007/s00011-011-0400-z
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000300292100002
URI http://repositorio.unifesp.br/handle/11600/34657

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