Diethylcarbamazine inhibits NF-κB activation in acute lung injury induced by carrageenan in mice
Autor: | Karla Patrícia Sousa Barbosa, Fabiana Oliveira dos Santos Gomes, Christina Alves Peixoto, Bruna dos Santos Silva, Gabriel Barros Rodrigues, Amanda Karolina Soares e Silva, Laise Aline Martins dos Santos, Maria Eduarda Rocha de França, Sura Wanessa Santos Rocha, Edlene Lima Ribeiro, Ingrid Tavares Fragoso, M.A.M. Donato, Teresinha Gonçalves da Silva |
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Rok vydání: | 2014 |
Předmět: |
Male
Transcriptional Activation MAPK/ERK pathway Curcumin Immunology Anti-Inflammatory Agents Inflammation Lung injury Pharmacology Carrageenan p38 Mitogen-Activated Protein Kinases Diethylcarbamazine Mice chemistry.chemical_compound Elephantiasis Filarial parasitic diseases medicine Animals Humans Immunology and Allergy Pulmonary Eosinophilia Pleurisy business.industry NF-kappa B NF-κB Disease Models Animal IκBα chemistry Inflammation Mediators medicine.symptom business Signal Transduction medicine.drug |
Zdroj: | International Immunopharmacology. 23:153-162 |
ISSN: | 1567-5769 |
Popis: | Diethylcarbamazine citrate (DEC) is widely used to treat lymphatic filariasis and Tropical Pulmonary Eosinophilia. A number of studies have reported a possible role in the host immune system, but exactly how DEC exerts this effect is still unknown. The present study reports the effects of DEC pretreatment on NF-κB regulation using the pleurisy model induced by carrageenan. Swiss male mice (Mus musculus) were divided into four experimental groups: control (SAL); carrageenan (CAR); diethylcarbamazine (DEC) and curcumin (CUR). The animals were pretreated with DEC (50 mg/kg, v.o), CUR (50 mg/kg, i.p) or distilled water for three consecutive days before pleurisy. One way analysis of variance (ANOVA) was performed by Tukey post-hoc test, and values were considered statistically significant when p < 0.05. DEC pretreatment reduced tissue damage and the production of inflammatory markers, such as NO, iNOS, PGE2, COX-2, and PARP induced by carrageenan. Similarly, a known inhibitor of NF-κB pathway (curcumin) was also able to reduce these parameters. Like curcumin, DEC prevents NF-κB activation by reducing NF-κB p65 phosphorylation and IκBα degradation. DEC prevented NF-κB activation via p38 MAPK, but did not interfere in the ERK pathway in this experimental model. However, further studies should be developed to confirm this hypothesis. These findings suggest that DEC could be a promising drug for inflammatory disorders, especially in pulmonary diseases such as Acute Lung Inflammation, due its high anti-inflammatory potential which prevents NF-κB activation. |
Databáze: | OpenAIRE |
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