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Mediators of Inflammation
Volume 2015 (2015), Article ID 265798, 12 pages
Research Article

Ouabain Modulates Zymosan-Induced Peritonitis in Mice

1Instituto de Ciências Biomédicas, Departamento de Farmacologia, Laboratório de Neurofarmacologia Molecular, Universidade de São Paulo, 05508-900 São Paulo, SP, Brazil
2Centro de Biotecnologia, Laboratório de Imunofarmacologia, Programa de Pós-Graduação em Fisiologia Multicêntrico, Universidade Federal da Paraíba, 58059-900 João Pessoa, PB, Brazil
3Instituto de Bioquímica Médica Leopoldo de Meis, Laboratório de Imunologia Tumoral, Universidade Federal do Rio de Janeiro, 21941-902 Rio de Janeiro, RJ, Brazil
4Laboratório de Biologia do Sistema Imune, Instituto de Microbiologia, Universidade Federal do Rio de Janeiro, 21941-902 Rio de Janeiro, RJ, Brazil
5Centro de Ciências da Saúde, Programa de Pós-Graduação em Produtos Naturais e Sintéticos Bioativos, Universidade Federal da Paraíba, 58059-900 João Pessoa, PB, Brazil

Received 20 March 2015; Accepted 22 April 2015

Academic Editor: Elzbieta Kolaczkowska

Copyright © 2015 Jacqueline Alves Leite et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Ouabain, a potent inhibitor of the Na+, K+-ATPase, was identified as an endogenous substance. Recently, ouabain was shown to affect various immunological processes. We have previously demonstrated the ability of ouabain to modulate inflammation, but little is known about the mechanisms involved. Thus, the aim of the present work is to evaluate the immune modulatory role of ouabain on zymosan-induced peritonitis in mice. Our results show that ouabain decreased plasma exudation (33%). After induction of inflammation, OUA treatment led to a 46% reduction in the total number of cells, as a reflex of a decrease of polymorphonuclear leukocytes, which does not appear to be due to cell death. Furthermore, OUA decreased TNF-α (57%) and IL-1β (58%) levels, without interfering with IL-6 and IL-10. Also, in vitro experiments show that ouabain did not affect endocytic capacity. Moreover, electrophoretic mobility shift assay (EMSA) shows that zymosan treatment increased (85%) NF-κB binding activity and that ouabain reduced (30%) NF-κB binding activity induced by zymosan. Therefore, our data suggest that ouabain modulated acute inflammatory response, reducing the number of cells and cytokines levels in the peritoneal cavity, as well as NFκB activation, suggesting a new mode of action of this substance.