作者: Yon Rojanasakul , Jiangping Ye , Fei Chen , Liying Wang , Ningli Cheng
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摘要: Tumor necrosis factor alpha (TNFalpha) plays an important role in the pathogenesis of silicosis and other chronic inflammatory lung diseases. The present study investigates nuclear transcription kappaB (NF-kappaB) oxygen free radicals silica-induced TNFalpha production primary alveolar macrophages RAW 264.7 cells. Using electrophoretic mobility shift assay (EMSA) enzyme-linked immunoadsorbent (ELISA), we have demonstrated that silica can induce NF-kappaB activation expression a dose-dependent manner. Transient transfection assays with plasmid construct containing binding sites linked to reporter gene further show is able transcriptional NF-kappaB-dependent gene. Inhibition by SN50, specific blocker, abolishes production. Pretreatment cells catalase (H2O2 scavenger) or deferoxamine (*OH effectively inhibits activation, whereas superoxide dismutase (O2 has opposite effect. These results indicate silica-mediated radical generation play roles expression.