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Objective: Pulmonary fibrosis is a serious hazard to human health in the respiratory system, a group of diseases. It is based on chronic wounds formation and deposition of extracellular matrix (extracelluar matrix, ECM) for the characteristics of the disease, which led to the destruction of the lung function and respiratory failure. That is, it is based on the excess of ECM production and deposition of diseases characterized by this process usually takes many years, and can cause lung damage and loss. The pathogenesis is not clear, the lack of effective clinical treatment options. Despite the irreversible formation of fibrosis, pulmonary fibrosis is a sexual chronic pathological process to find a new intervention targets to explore the molecular mechanisms of the pathogenesis of pulmonary fibrosis, delay or block the progress of pulmonary fibrosis. In the the fibrosis development process, transforming growth factor-β (transforming growth factor-β, TGF-β) promote fibrosis is yes. TGF-β-induced fibroblast synthesis and accumulation of ECM, a long time, it was seen as an important fibrotic response regulator. TGF-β is generated through the regulation of ECM cell transcriptional or post-transcriptional level, and promote the expression of various ECM and can be induced into fibroblasts and other cells to synthesize and secrete extracellular matrix proteins and inhibit its degradation. However, TGF-β-mediated fibrosis response signal transduction pathway, by TGF-β to its receptor binding was to achieve the activation of the signal pathway, to thereby induce a series of signal transduction processes, to achieve it's biological effects. Dependence on TGF-β receptor type II transforming growth factor-β (transforming growth factor-β II type receptor, TGF-βR Ⅱ) play a role, only the two signal transduction pathways induced upon binding to the cell surface. Studies show, TGF-βR Ⅱ TβR-Ⅱ, ActR-Ⅱ, ActR-Ⅱ B, BMPR-Ⅱ and AMHR-Ⅱ five subtypes, but what subtype of what factors are involved in the process of the formation of pulmonary fibrosis, not yet clear. In this study, bleomycin (bleomycin, BLM)-induced pulmonary fibrosis in rats as a model observed pulmonary fibrosis TGF-βR Ⅱ subtype expression changes, provide intervention targets for future clinical treatment of pulmonary fibrosis . Methods: Animals: 6 weeks old SD rats, females, weight 180g-220g. 2. Preparation of animal model: rats after ether anesthesia, anterior exposed trachea intratracheal injection of 0.4% BLM saline injection (5mg/kg). 3 groups: two groups, each group 36 rats. (1) pulmonary fibrosis group (F stands for) is divided into six subgroups: F1, F3, F7, F14, F28, F35 group, representing give BLM 1,3,7,14,28,35 days put to death; (2) normal control group (N stands for): Take the same period rats were sacrificed. 4. Research methods: application hematoxylin - eosin (HE) staining of lung tissue morphological changes in the application of real-time fluorescence quantitative PCR (real-time PCR) analysis of lung tissue expression of TGF-βR Ⅱ subtype. Results: 1 light microscope pathomorphology observed (HE staining): pulmonary fibrosis model was successfully given BLM 1,3,7,14,28,35 fibrosis became clear. Real-time PCR analysis of TGF-βR Ⅱ groups at different stages of lung tissue the subtypes of expression changes: the ActR-II A and the ActR-Ⅱ B fibrogenesis express lower expression level of the highest stage less than control group doubled, whereas TβR-Ⅱ in a high expression level in the first days after the given BLM i.e. to reach the first peak, and then in the first seven days, and then gradually decreased to the 28th day of the expression level for the lowest state near baseline, and subsequently increased to 35 days is still at a high level. AMHR-Ⅱ one day after giving BLM began to rise, peaked to 14 days, then decreased gradually, in the first 28 days and 35 days down near the baseline. Fibrosis group expression of TβR-II, the ActR-II A, the ActR-II B and AMHR-Ⅱ compared with normal control group, P lt; 0.05, with statistical significance. Fibrosis group factor comparison, only TβR-Ⅱ factor than other factors, P lt; 0.05, statistically significant, while other factors compared with each other, P gt; 0.05, not statistically significant. Conclusion: 1.TβR-II, the ActR-II A, ActR-II B and AMHR-II are involved in the formation of pulmonary fibrosis. 2.TβR-Ⅱ formed early during the inflammatory response and fibrosis showed high expression levels of the late, its higher multiples of up to seven times the normal control group.
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