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Mediators of Inflammation
Volume 2013, Article ID 164202, 13 pages
http://dx.doi.org/10.1155/2013/164202
Research Article

Anti-Inflammatory Effects of Ellagic Acid on Acute Lung Injury Induced by Acid in Mice

1Laboratório de ImunoFarmacologia Experimental (LIFE), Universidade Federal do Triângulo Mineiro (UFTM), Departamento de Clínica Médica, Instituto de Ciências da Saúde, Uberaba MG, Brazil
2Departamento de Farmacologia, Universidade Federal de Santa Catarina, Florianópolis, SC, Brazil
3Departamento de Análises Clínicas, Toxicológicas e Bromatológicas, Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo (USP), Ribeirão Preto, SP, Brazil
4Departamento de Clínica Médica, Universidade Federal do Triângulo Mineiro, Rua Manoel Carlos 162, 38025-380 Uberaba, MG, Brazil

Received 12 November 2012; Accepted 23 December 2012

Academic Editor: Nina Ivanovska

Copyright © 2013 Daniely Cornélio Favarin 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.

Abstract

Acute lung injury (ALI) is characterized by alveolar edema and uncontrolled neutrophil migration to the lung, and no specific therapy is still available. Ellagic acid, a compound present in several fruits and medicinal plants, has shown anti-inflammatory activity in several experimental disease models. We used the nonlethal acid aspiration model of ALI in mice to determine whether preventive or therapeutic administration of ellagic acid (10 mg/kg; oral route) could interfere with the development or establishment of ALI inflammation. Dexamethasone (1 mg/kg; subcutaneous route) was used as a positive control. In both preventive and therapeutic treatments, ellagic acid reduced the vascular permeability changes and neutrophil recruitment to the bronchoalveolar lavage fluid (BALF) and to lung compared to the vehicle. In addition, the ellagic acid accelerated the resolution for lung neutrophilia. Moreover, ellagic acid reduced the COX-2-induced exacerbation of inflammation. These results were similar to the dexamethasone. However, while the anti-inflammatory effects of dexamethasone treatment were due to the reduced activation of NF-κB and AP-1, the ellagic acid treatment led to reduced BALF levels of IL-6 and increased levels of IL-10. In addition, dexamethasone treatment reduced IL-1β. Together, these findings identify ellagic acid as a potential therapeutic agent for ALI-associated inflammation.