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J Ethnopharmacol ; 103(3): 372-8, 2006 Feb 20.
Artículo en Inglés | MEDLINE | ID: mdl-16183225

RESUMEN

We demonstrate that polysaccharides isolated from Salicornia herbacea (Salicornia polysaccharides, SPS) significantly induces nitric oxide (NO) production and inducible NO synthase (iNOS) transcription through the activation of nuclear factor-kappaB/Rel (NF-kappaB/Rel). SPS dose-dependently induced the production of NO in isolated mouse peritoneal macrophages and RAW 264.7, a mouse macrophage-like cell line. Moreover, iNOS gene expression was strongly induced by SPS in RAW 264.7 cells. To further investigate the mechanism responsible for the induction of iNOS gene expression, we investigated the effect of SPS on the activation of transcription factors including NF-kappaB/Rel and Oct, whose binding sites were located in the promoter of iNOS gene. Treatment of RAW 264.7 cells with SPS produced strong induction of NF-kappaB/Rel-dependent reporter gene expression, whereas Oct-dependent gene expression was not affected by SPS. Nuclear translocation and DNA binding activity of NF-kappaB/Rel was significantly induced by SPS. The treatment with NF-kappaB SN50, an inhibitor of NF-kappaB/Rel nuclear translocation, effectively inhibited the activation of NF-kappaB/Rel binding complexes and NO production. In conclusion, we demonstrate that SPS stimulates macrophages to express iNOS gene through the activation of NF-kappaB/Rel.


Asunto(s)
Chenopodiaceae/química , Activación de Macrófagos , Macrófagos Peritoneales/efectos de los fármacos , Polisacáridos/farmacología , Animales , Línea Celular , Relación Dosis-Respuesta a Droga , Medicamentos Herbarios Chinos , Femenino , Regulación de la Expresión Génica , Macrófagos Peritoneales/inmunología , Ratones , FN-kappa B/antagonistas & inhibidores , FN-kappa B/metabolismo , Óxido Nítrico/metabolismo , Óxido Nítrico Sintasa de Tipo II/genética , Óxido Nítrico Sintasa de Tipo II/metabolismo , Péptidos/farmacología , Polisacáridos/aislamiento & purificación , Proteínas Proto-Oncogénicas c-rel/metabolismo , ARN Mensajero/metabolismo
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