(1) The replication method adopts the non-exposed intratracheal injection method. Each rat is injected with 1ml silica dust suspension (prepared with normal saline to make 50g/L suspension, sterilized and added with penicillin 2×1000000U/L), stain After the dust was over, the animals were sacrificed on the 28th day, and the lung tissues were grossly examined. Rat lung tissue specimens were taken and fixed with fixative solution to make conventional pathological tissue sections and ultra-thin sections under transmission electron microscopy, respectively, under light and electron microscopes Observed.
(2) Characteristics of the model. It can be seen from the naked eye that the lungs of the model rat have scattered gray-white nodules with the size of the needle tip, which are relatively evenly distributed and feel grit to the touch. Microscopic histopathological observation shows that there is a small focal interstitial inflammation in the lung tissue, mainly by lymphocytes and macrophages, and there are many cell nodules; the nodules are mostly composed of macrophages and fibroblasts In some nodules, foreign body giant cells and a small amount of collagen fibers can be seen, and the nodules are fused with each other, and there is mild fibrous tissue hyperplasia around them; in the lung tissue, there are different degrees of alveolar type II epithelial cell hyperplasia, with cell knots. The alveolar wall near the nodular lesion is more obvious, which is in line with the early pathological characteristics of patients with clinical silicosis; the hyperplastic alveolar type II cells are cuboidal, enlarged in volume, projecting to the cell cavity, rich in cytoplasm, lightly colored, and visible vacuoles Formation; the nucleus is round, the chromatin is fine, and the hyperplasia is marked into a glandular cavity-like structure. Electron microscopic observation of hyperplastic alveolar type Ⅱ epithelial cells has microvilli on the free surface, a large number of lamellar bodies in the cytoplasm, and some lamellar bodies are vacuolated, mitochondria, rough endoplasmic reticulum and Golgi complex rich. The results of immunohistochemistry and immunoelectron microscopy showed that transforming growth factor β1 (TGFβ1) and platelet-derived growth factor-B (PDGF-B) gene positives and enzyme-labeled particles were all located in the cytoplasm of alveolar type II epithelial cells.
(3) Comparative medicine Alveolar type Ⅱ epithelial cell hyperplasia is one of the early pathological changes of silicosis. In the past, it was difficult to distinguish alveolar type Ⅱ epithelial cells and macrophages with conventional paraffin sections and simple light microscope observation, thus neglecting alveolar type Ⅱ The presence of epithelial cells. This model shows that there are indeed alveolar type II cell hyperplasia and active function in the early lesions of experimental silicosis. In the process of silicosis fibrosis, alveolar type Ⅱ cells, macrophages and mast cells form a complex cell network. Alveolar type Ⅱ cells may be mainly involved in the early pathological changes of silicosis, while macrophages and mast cells are Fibrotic lesions play a role in the continued development.