矽肺动物模型的病理观察  

Pathologic observation on animal model of silicosis

作　　者：蒲新明 温浩[2] 窦红 徐志新[2] 刘培成 李赛君 白鸥 吴新 苏汉新 刘新军 江瑞康 张劬 

机构地区：[1]新疆维吾尔自治区职业病医院,乌鲁木齐830091 [2]新疆医科大学第一附属医院,乌鲁木齐830091

出　　处：《中华劳动卫生职业病杂志》2011年第10期761-765,共5页Chinese Journal of Industrial Hygiene and Occupational Diseases

基　　金：中国煤矿尘柿病治疗基金会（200807）;新疆维吾尔自治区科学研究和技术开发（含攻关）项目[项目编号：200633128;课题编号：200633128（1）]

摘　　要：目的 探讨二氧化硅致大鼠及贵州小香猪肺组织纤维化的变化。方法 采用非暴露法建立SD大鼠、贵州小香猪矽肺动物模型，光学显微镜及透视电镜下观察其肺内病理变化，免疫组化法观察肺组织中细胞因子的表达。结果（1）大鼠及猪矽肺模型主要形态学变化：染尘7～15d，在肺泡腔内可见矽尘、大量的巨噬细胞、尘细胞、肺上皮细胞及少量的中性粒白细胞，形成巨噬细胞肺泡炎及I级结节；染尘30～90d，肺组织的呼吸性细支气管及肺泡内、小叶问隔、血管及支气管周围、胸膜下形成I一Ⅲ级结节，少数动物模型可见Ⅳ级结节，伴淋巴细胞浸润。（2）大鼠及贵州小香猪肺组织中细胞角蛋白（CK）、肺表面活性物质相关蛋白A（sP—A）、吞噬细胞（CD68）、碱性成纤维细胞因子（b—FGF）、肿瘤坏死因子（TNFa）、白细胞介素-6（IL一6）、转化生长冈子（TGFβt）、NF-kB／P50、NF-KB／P65、血管内皮生长因子（VEGF），随着染尘时间的延长，表达逐渐减弱，但仍高于对照组。60～90dCD68仍呈阳性表达。（3）电镜观察肺泡上皮和巨噬细胞的变化：在SiO2：刺激下，肺泡I型上皮脱落，Ⅱ型上皮细胞及巨噬细胞增生，且细胞功能活跃。结论建立的大鼠及猪肺纤维化模型符合巨噬细胞肺泡炎至纤维化的演变过程。Objective To explore the pathological changes of pulmonary fibrosis induced by SiO2 in rats and pigs. Methods The silicosis models in rats and pigs were established by non-exposure method. The pathologic changes in lung tissues of rats and pigs were observed with HE staining under a light microscopy and under a transmission electron microscopy （TEM）, the expression of cytokines was detected by immunohisto- chemistry. Results （1） The main pathologic changes of silicosis models in rats and pigs included： in 7-15 days after treatment, silica dusts, dust cells, a lot of macrophages, lung epithelial cells, a few neutrophils, macrophage alveolar inflammation and nodules of stage I were found in alveolar space; in 30-90 days after treatment, many nodules of stage I -Ill or lVwith lymphocytes infihration were observed in respiratory bronchi- oles, alveoli, interlobular septa, the subpleural and around blood vessels and bronchi. （2） The expression levels of CK protein, SP-A protein, CD68, b-FGF, TNF-c~, IL-6, TGF-[31, NFKappa/P50, Kappa/P65 and VEGF re- duced with exposure time, but still were higher than those of the control. （3） The shed alveolar type I cells, pro- liferation of alveolar type ]I ceils or macrophages and activated cellular function induced by silica were observed under TEM. Conclusion The development of pulmonary fibrosis in silicosis models corresponded with the pro- cess from macrophages alveolar inflammation to pulmonary fibrosis.

关 键 词：矽肺 模型 动物 肺纤维化 病理学 

分 类 号：R135.2[医药卫生—劳动卫生]