一氧化氮与矽肺早期炎性损伤

综述了一氧化氮 (NO)参与矽肺损伤的细胞和分子机制。大量资料表明 ,NO与矽肺的形成有关。作为一种自由基 ,NO不仅损伤肺组织 ,而且与超氧阴离子结合 ,形成毒性更强的过氧亚硝酸阴离子 ,它通过不同机制在肺内产生广泛的细胞毒性。NO的产生需要细胞因子的存在。NF κB在诱导型一氧化氮合酶基因表达过程中的作用尤其重要。有关NO在NF κB激活过程中的作用 ,目前文献报道存在分歧

Nitric oxide and early inflammatory injury in silicosis

There is a body of evidence that NO formation could be implicated in mediating silica-induced pulmonary fibrosis. As a reactive free radical, NO may not only contribute to lung parenchymal tissue injury but also has the ability to combine with superoxide and form a highly reactive toxic species-peroxynitrite, which can induce extensive cellular toxicity via a variety of mechanisms in the lung tissues. Several cytokine is required for NO production. NF-kappa B plays a particularly important role in the regulation of gene expression of the iNOS isoform. There are discrepancy between the current literature regarding the role NO in the NF-kappa B activation and therefore, in this paper, the role of NO in the cellular and molecular mechanisms of silica-induced lung damage was reviewed.