The animal model of silicosis of non-exposed tracheal instillation induced by SiO2 in rats lung fibrosis were studied. To investigate:Methods
Ninety-six healthy male Sprague-Dawley (SD) rats weighing 180~220 g were randomly divided into normal saline group (n=32), silicosis model group (n=32), PolyG prevention group (n=16) and PolyG (28 days) treatment group (n=16). After the rats were anaesthetised with ether, the control group was injected with 1 ml normal saline by bronchial instillation. The rats in other groups were treated with non-exposed tracheal infusion of a one-time infusion of 50 ml/L silica suspension 1 ml. The rats in the PolyG preventive group were treated with PolyG 2.5 mg/kg body weight (the weight of each rat was determined 28 days after modelling) at the same time by tail vein injection. The rats in the PolyG treatment group were treated with intravenous injection of PolyG 2.5 mg/Kg body weight (by modelling 28 days after each rat weight to determine the appropriate dose). The rats in the polyG prevention group and the treatment group were sacrificed on the 28th day and the 56th day after the corresponding administration. Silicosis model group and saline control group also have 8 rats were sacrificed at the same time point.(Macrophage receptor with collagenous structure, MARCO), E-cadherin (E-cadherin) were detected by Western blotting. The macrophage receptor (MARCO) Cadherin, E-cadherin, α-smooth muscle actin (α-SMA), vimentin and type I and type III collagen; the right amount of lung tissue, The relative expression levels of E-cadherin, α-SMA, vimentin and type I and type III procollagen mRNA were detected by Real-time PCR. The right middle lobe tissue was fixed with 4% paraformaldehyde, paraffin section, the histopathological changes of lung tissue were observed by HE staining and Masson staining. Immunohistochemical staining was used to detect the localization and expression of E-cadherin, α-SMA and vimentin in lung tissue.