Brabykinin B1 Receptor Antagonism Is Beneficial in Renal Ischemia-Reperfusion Injury

Brabykinin B1 Receptor Antagonism Is Beneficial in Renal Ischemia-Reperfusion Injury

Autor Wang, Pamella H. M. Autor UNIFESP Google Scholar
Campanholle, Gabriela Google Scholar
Cenedeze, Marcos A. Autor UNIFESP Google Scholar
Feitoza, Carla Q. Autor UNIFESP Google Scholar
Goncalves, Giselle M. Autor UNIFESP Google Scholar
Landgraf, Richardt G. Google Scholar
Jancar, Sonia Google Scholar
Pesquero, Joao B. Autor UNIFESP Google Scholar
Pacheco-Silva, Alvaro Autor UNIFESP Google Scholar
Câmara, Niels Olsen Saraiva Autor UNIFESP Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
Universidade de São Paulo (USP)
Resumo Previously we have demonstrated that bradykinin B1 receptor deficient mice (B1KO) were protected against renal ischemia and reperfusion injury (IRI). Here, we aimed to analyze the effect of B1 antagonism on renal IRI and to study whether B1R knockout or antagonism could modulate the renal expression of pro and anti-inflammatory molecules. To this end, mice were subjected to 45 minutes ischemia and reperfused at 4, 24, 48 and 120 hours. Wild-type mice were treated intra-peritoneally with antagonists of either B1 (R-954, 200 mg/kg) or B2 receptor (HOE140, 200 mg/kg) 30 minutes prior to ischemia. Blood samples were collected to ascertain serum creatinine level, and kidneys were harvested for gene transcript analyses by real-time PCR. Herein, B1R antagonism ( R-954) was able to decrease serum creatinine levels, whereas B2R antagonism had no effect. the protection seen under B1R deletion or antagonism was associated with an increased expression of GATA-3, IL-4 and IL-10 and a decreased T-bet and IL-1b transcription. Moreover, treatment with R-954 resulted in lower MCP-1, and higher HO-1 expression. Our results demonstrated that bradykinin B1R antagonism is beneficial in renal IRI.
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: 04/08311-6
FAPESP: 05/50085-6
FAPESP: 06/03982-5
FAPESP: 07/07139-3
CNPq: 04/08311-6
CNPq: 05/50085-6
CNPq: 06/03982-5
CNPq: 07/07139-3
Data 2008-08-25
Publicado em Plos One. San Francisco: Public Library Science, v. 3, n. 8, 9 p., 2008.
ISSN 1932-6203 (Sherpa/Romeo, fator de impacto)
Editor Public Library Science
Extensão 9
Direito de acesso Acesso aberto Open Access
Tipo Artigo
Web of Science WOS:000264429000003

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