Desaki M, Takizawa H, Kasama T, Kobayashi K, Morita Y, Yamamoto K
Department of Respiratory Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Cytokine. 2000 Aug;12(8):1257-60. doi: 10.1006/cyto.2000.0704.
Recent studies indicate that interleukin 8 (IL-8) plays an important role in interstitial lung diseases including silica-induced lung inflammation. To investigate the regulation of IL-8 expression and production in human bronchial epithelial cells, we examined the effects of silica on NF-kappaB activation. Human bronchial epithelial cell line BET-1A was cultured with hormonally defined Ham's F12 medium. The administration of silica induced IL-8 production in BET-1A dose-dependently and time-dependently. Northern blot analysis demonstrated that silica upregulated IL-8 expression in BET-1A. Moreover, electrophoretic mobility shift assays revealed that NF-kappaB activation occurred in the presence of silica, which was inhibited by antioxidants such as N-acetylcysteine (NAC). These data suggest that reactive oxygen species may be involved in the activation of NF-kappaB induced by silica.
最近的研究表明,白细胞介素8(IL-8)在包括矽肺诱导的肺部炎症在内的间质性肺疾病中起重要作用。为了研究人支气管上皮细胞中IL-8表达和产生的调节机制,我们检测了二氧化硅对核因子κB(NF-κB)激活的影响。人支气管上皮细胞系BET-1A用含有激素的Ham's F12培养基培养。二氧化硅的给药在BET-1A中剂量依赖性和时间依赖性地诱导IL-8产生。Northern印迹分析表明,二氧化硅上调了BET-1A中IL-8的表达。此外,电泳迁移率变动分析显示,在有二氧化硅存在的情况下发生了NF-κB激活,而这种激活被抗氧化剂如N-乙酰半胱氨酸(NAC)所抑制。这些数据表明,活性氧可能参与了二氧化硅诱导的NF-κB激活。