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研究表明,当暴露于矽尘等炎性刺激物作用时,肺泡巨噬细胞和肺中性粒细胞一氧化氮(nitricoxide,NO)生成增加,并上调诱导型一氧化氮合酶(inducible nitric oxide,iNOS)基因表达。但是,有研究认为矽尘并不能够直接增加培养的肺泡巨噬细胞产生NO;还有研究认为NO可能是肺纤维性结节形成的调节因子。这些研究提示NO及NOS的变化与矽尘对肺的作用有关。本研究测定了染尘后不同处理时点肺匀浆NO含量和NOS活力,并进行相关分析,以期能有助于解释矽尘对肺的作用。
Studies have shown that when exposed to inflammatory stimuli such as silica dust, the production of nitric oxide (NO) in alveolar macrophages and pulmonary neutrophils is increased and the up-regulation of inducible nitric oxide (inducible nitric oxide , iNOS) gene expression. However, some studies suggest that silica dust does not directly increase the production of NO in cultured alveolar macrophages. There is also research that NO may be a regulator of pulmonary fibrosis. These studies suggest that changes in NO and NOS are related to the effects of silica dust on the lungs. In this study, NO content and NOS activity in lung homogenate were determined after different treatments, and the correlation analysis was conducted in order to help explain the effect of silica dust on lung.