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目的 探讨肺泡Ⅱ型细胞增生在矽肺纤维化中的意义。方法 建立大鼠实验性矽肺早期病变模型 ,光镜和电镜观察其肺内病变及肺泡Ⅱ型细胞增生 ;用免疫组织化学、原位杂交、免疫电镜、原位杂交与免疫组织化学双标技术检测其肺泡Ⅱ型细胞内转化生长因子 β1(TGFβ1)和血小板源性生长因子 B(PDGF B)的基因表达。结果 ( 1)大鼠矽肺模型主要形态学改变 :灶性间质性炎症 ,细胞结节和轻度纤维组织增生 ,肺泡Ⅱ型细胞明显增生。 ( 2 )实验组大鼠增生的肺泡Ⅱ型细胞内TGFβ1、PDGF BmRNA和蛋白表达增强 ;对照组大鼠仅有部分正常肺泡Ⅱ型细胞TGFβ1mRNA呈弱阳性 ,未见TGFβ1蛋白、PDGF BmRNA和蛋白表达。结论 肺泡Ⅱ型细胞增生是矽肺早期的病变之一 ;增生的肺泡Ⅱ型细胞TGFβ1和PDGF B基因表达上调 ,在矽肺纤维化的早期病变中可能起重要作用。
Objective To investigate the significance of alveolar type Ⅱ cell proliferation in silicotic fibrosis. Methods The experimental model of silicotic early lesions was established in rats. The pathological changes of lungs and the proliferation of alveolar type Ⅱ cells were observed under light microscope and electron microscope. The expression of type Ⅱ cells was detected by immunohistochemistry, in situ hybridization, immunoelectron microscopy, in situ hybridization and immunohistochemistry The gene expression of transforming growth factor-β1 (TGFβ1) and platelet-derived growth factor B (PDGF B) in alveolar type II cells were detected. Results (1) The main morphological changes of silicosis model in rats: focal interstitial inflammation, cell nodules and mild fibrous tissue hyperplasia, alveolar type Ⅱ cells hyperplasia. (2) The expression of TGFβ1, PDGF BmRNA and protein in the alveolar type Ⅱ cells in the experimental group were enhanced; only the TGFβ1 mRNA in the normal alveolar type Ⅱ cells in the control group was weakly positive, but there was no TGFβ1, PDGF BmRNA and protein expression . Conclusions Alveolar type Ⅱ cell hyperplasia is one of the early lesions of silicosis. The upregulation of TGFβ1 and PDGF B gene expression in hyperplastic alveolar type Ⅱ cells may play an important role in the early stage of silicosis.