自由基在矽肺发病机制中的作用

为探讨自由基在矽肺发病机制中的作用,叙述了自由基的来源及其对肺巨噬细胞(AM)和细胞因子分泌、肺内其他生物基质、免疫的作用.石英在粉碎过程中自身可产生自由基;当AM吞噬石英和游走时引起"呼吸爆发",可产生大量自由基;髓单核细胞在肺中转化为AM后被活化时还可产生氮氧自由基.自由基作用于AM,产生脂质过氧化导致质膜损伤,进而分泌多种细胞因子,诱导纤维细胞增生和胶原合成,造成肺纤维化.自由基还可以作用于肺内其他生物基质和对免疫功能发生影响,促进肺纤维化过程.可见,自由基在矽肺发病机制中具有重要作用.

Role of Free Radical in Pathogenesis of Silicosis

The role of the free radical in the pathogenesis of silicosis has been reviewed. The source of free radical and its action on the alveolar macrophage and the secretion of cytokine, other biological matrix and immunity functions were described. Free radical can be produced during the smashing process of silica. Free radical can result from the "respiratory burst", which occurs after the alveolar macrophage swallows silica and moves. The nitrogenic and oxygenic free radical can be produced during the activation of alveolar macrophage. The action of free radical on the alveolar macrophage will result in lipid peroxidation. The plasma membrane damage is caused and will secret various cytokines. Then cytokines can induce the hyperplasia of fibroblast and the synthesis of collagen. Finally lung fibrosis will occur. In addition, free radical can also act on other biological matrix and affect the immunity functions, which will promote the process of the lung fibrosis.