Effects Of Lung Fibrosis On Lung Microvessel Density, ALK And Other Factors In Lung Fibrosis Rats And Its In Vitro Cell

Objective:Through to the research on whole animal experiment and cells experiment in vitro, can explore the abnormal angiogenesis in the pathogenesis of IPF, and the treatment of FXF in IPF.Method:Animal experiment:156 rats were randomly divided into 7 groups:control group and 12, model group and 24, FXF high-dose group and 24, FXF dosage group of 24, FXF low-dose group and 24, the western medicine control group were divided into two groups:losartan group 24, prednisone group 24.Saline perfusion in false operation group, the rest rats were infused BLM to induce model disease through tracheal intubation,3mg/kg. Intragastric administration started from the next day after inducing model disease. Instragastric volume: FXF big, middle, small dose group were 2.4g/kg,1.2g/kg,0.6g/kg. Losartan group, prednisone group 5mg/kg 10mg/kg. The rats were deal with on 14 and 28 days after inducing model disease respectively. The left lung were tested through histopathology examination with HE staining and MAS SON staining, Semi quantitative detection had been introduced to figure out the degree of alveolitis and pulmonary fibrosis. To obvious cell ultrastructure with electron microscope. Immunohistochemical method to detect the expression of CD31, CD34, VEGFR1, VEGFR2, ALK, PI3K, P38. Through the analysis of each group in the protein expression of the situation, in order to understand abnormal angiogenesis about the lung tissue of pulmonary fibrosis in rat under the corresponding intervention measures, and FXF intervention into angiogenesis, inflammation reaction pathways as well as the damage after repair pathways, and then clear FXF in the role of anti fibrosis.Cells experiment in vitro:Separation of 28 days microvascular endothelial cells from bleomycin induced pulmonary fibrosis of rats, with FXF large, medium, small, Losartan and prednisone to stimulate cells. RT-PCR method is used to detect VEGF and VEGFR, ALK, P38, PI3K gene expression.Results:Animal experiment:The pathological tissue about FXF groups of rats under electron microscope showed that the degree of inflammation and collagen fibers deposition conditions significantly decrease trend in the model group, so FXF can inhibit the inflammation and collagen deposition. The CD31, CD34 expression from FXF group was significantly reduced compared with model group. It shows that FXF can inhibit angiogenesis; By inhibiting VEGF/VEGFR1, VEGFR2 signaling pathways conduction, inhibit angiogenesis; By inhibiting the TGF-β/ALK the activation of signaling pathways, thereby inhibit collagen synthesis and deposition, and does not interfere with the degradation of extracellular matrix; Through the inhibition of PI3K/Akt signaling pathway, decrease of collagen synthesis in order to slow the progress of pulmonary fibrosis; By inhibiting the generation of P38 lightning, so as to control its regulation of neutrophils and endothelial cells, reduce the inflammatory reaction and inhibit the progress of the pulmonary fibrosis.Cells experiment in vitro:FXF group can inhibit the expression of VEGF, thus inhibiting angiogenesis pathway, achieve the goal of control of pulmonary fibrosis. Prednisone, Losartan can inhibit the expression of VEGFR, which affect VEGF/VEGFR pathway conduction, to control the progress of the pulmonary fibrosis.P38 gene expression results show that the treatment group in the cell in vitro experiments can inhibit the expression of P38, so as to reduce inflammation, relieve the progress of the pulmonary fibrosis, and FXF high-dose group of obvious advantages.Conclusion:FXF can inhibit the inflammation of pulmonary fibrosis, inhibit the hyperplasia of abnormal blood vessels, improving the extracellular matrix and collagen fiber formation and deposition, and slow the process of pulmonary fibrosis.