Your browser doesn't support javascript.
loading
Inhibitory effect of dexamethasone on myeloid differentiation factor 88 and tumor necrosis factor-alpha expressions in mouse peritoneal macrophages / 南方医科大学学报
Article em Zh | WPRIM | ID: wpr-325105
Biblioteca responsável: WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To study the inhibitory effect of dexamethasone (DEX) on myeloid differentiation factor 88 (MyD88) and tumor necrosis factor-alpha (TNF-alpha) expression in mouse peritoneal macrophages in innate immune response to Penicillium marneffei (PM).</p><p><b>METHODS</b>Mouse peritoneal macrophages were cultured in the presence of heat-inactivated yeast-phase PM with or without DEX, and the protein and mRNA expressions of MyD88 in the macrophages were detected using Western blotting and real-time PCR, respectively. TNF-alpha in the cell culture supernatant was measured with enzyme-linked immunosorbent assay.</p><p><b>RESULTS</b>DEX suppressed TNF-alpha production by the macrophages co-cultured with PM. The expressions of MyD88 were up-regulated by PM stimulation, whose effect was inhibited by the application of DEX.</p><p><b>CONCLUSION</b>The inhibitory effect of DEX on PM-induced proinflammatory responses of the macrophage is directly associated with the inhibition of MyD88 expression.</p>
Assuntos
Texto completo: 1 Índice: WPRIM Assunto principal: Penicillium / Farmacologia / Dexametasona / Células Cultivadas / Fator de Necrose Tumoral alfa / Macrófagos Peritoneais / Biologia Celular / Fator 88 de Diferenciação Mieloide / Genética / Metabolismo Limite: Animals Idioma: Zh Revista: Journal of Southern Medical University Ano de publicação: 2009 Tipo de documento: Article
Texto completo: 1 Índice: WPRIM Assunto principal: Penicillium / Farmacologia / Dexametasona / Células Cultivadas / Fator de Necrose Tumoral alfa / Macrófagos Peritoneais / Biologia Celular / Fator 88 de Diferenciação Mieloide / Genética / Metabolismo Limite: Animals Idioma: Zh Revista: Journal of Southern Medical University Ano de publicação: 2009 Tipo de documento: Article