Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 1 de 1
Filtrar
Más filtros











Base de datos
Intervalo de año de publicación
1.
J Sci Food Agric ; 93(3): 646-51, 2013 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-23015382

RESUMEN

BACKGROUND: Propolis is a bee product with various biological properties, including an antiviral activity when taken orally. However, its mechanisms at the cellular and molecular level are not well understood. RESULTS: We investigated the effect of propolis on antiviral signaling in A549 cells transfected with double-stranded RNA (dsRNA), a model for viral infection. Pretreatment of the cells with propolis inhibited poly I:C (synthetic dsRNA)-induced interferon (IFN)-ß expression. Propolis had no effect on the dsRNA-induced expression of RIG-I-like receptors (RLRs), which are known as intracellular viral RNA sensors. As to the effect on antiviral executor genes, propolis enhanced myxovirus resistance 1 (MX1) expression, whereas interferon-inducible gene 6-16 (G1P3) and 2'-5'-oligoadenylate synthetase (OAS) were unaffected. All of these genes belong to the IFN-inducible genes, suggesting that the effect of propolis on antiviral signaling is not necessarily mediated by the autocrine regulation by IFN-ß. Propolis pretreatment inhibited dsRNA-induced interleukin-8 (IL8) and CCL5 expression, and consequently lowered polymorphonuclear leukocyte (PMN) chemotactic activity in the cell-conditioned medium. CONCLUSION: Taken together, these results suggest that propolis may suppress excess inflammatory responses without affecting the innate immunity during viral infection.


Asunto(s)
Antivirales/farmacología , Interferón beta/genética , Neutrófilos/efectos de los fármacos , Própolis/farmacología , ARN Bicatenario/antagonistas & inhibidores , Adenocarcinoma , Brasil , Línea Celular Tumoral , Quimiotaxis de Leucocito/efectos de los fármacos , Medios de Cultivo Condicionados , Expresión Génica/efectos de los fármacos , Humanos , Interferón beta/antagonistas & inhibidores , Neoplasias Pulmonares , Neutrófilos/fisiología , Poli I-C/antagonistas & inhibidores , Poli I-C/farmacología , ARN Bicatenario/fisiología , Transfección
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA