| Activition of fibroblasts,proliferation and accumulation of a great deal of extra-cell metrix are the primary pathological characteristic of pulmonary fibrosis. Multiple factors can cause pulmonary fibrosis such as professional dust(SiO2 et al),virus(coral virus et al),radiational injury and some medicine(bleomycin et al). Besides, one kind of pathodenesis-unclear pulmonary fibrosis-idiologic pulmonary fibrosis. Although those pathogenesis is unclear, fibrostic development and result are same basicly. Present the detail mechanism is still unclear and the dramatic advance on its early effective prevention and treatment have still not be got. This experiment was performed in two levels including cells and animals. Animal model of pulmonary fibrosis was established by y -ray irradiation and bleomycin inducing. Pulmonary fibrosis mechanism was explored and its preventive and treatment role using taurine, arginine, IBE5 and rh- INF with Chinese phenotype were performed. HPF was divided into group control,irradiation,medicine administration(tau,arg or IBE5 0.1 , 1 10ug.ml-1 -INF 0.05, 0.1 0.5, lug/ml), imaging analysis was performed after MTT and immunocytochemistry.26 male mice was randoem divided into group Ctr,tau,arg,medicine was given by drinking three day before irradiation in two preventive groups for two months in a concentration of 10g.ml-1, lung sample was obtained in 1,3,6 months after irradiation. 42 C57 mice were divided into 5 groups: normal control,BLM,IBE5 0.025 g.kg-1.d-1, IBE5 0.05 g.kg-1.d-1, IBE5 0.1g.kg-1.d-1.IBE5 was administrated into stomach after resolution.BLM was injected into bronchus 4day after IBE5 was added. IBE5 was kept for 30 days. 50 C57 male mice was divided into group Ctr, BLM, INF- 0.25 ug. d-1, 0. 5 ug. d-1, 1.0ug. d-1, different doses of INF- was injected by ip 3day before model establish for 35 days. When sample was got, left lung was homogenated for Hyp, right lung was sectioned into slides for HE, serus red and immunocytochemic staining as well as imaging analysis.Cellular test result was shown that tau, arg, IBE5 and INF could inhibit abnormal proliferation of human fibroblasts stimulated by irradiation to lungs, decrease cellular a - SMA MMP-7 expression. In two kind of pulmonary fibrotic models, we found that interstitial neumonia was appeared in early stage and pulmonary fibrosis was formed in late stage.After tau, arg, IBE5 and INF were administrated, PF was inhibited in a different content, a -SMA was expressed only in the smooth muscles of vessel, bronchus walls;MMP-7 and MMP-9 were expressed only in bronchial epithelia.In fibrotic pulmonary tissue, a -SMA expression was increased which mainly located in myofibroblasts especially beside the vessel and bronchile.The MMP-7 had a positive ratio to fibrotic content which was shown as positive signal in bronchiol epithelial, phagocyte and myofibroblast by immunocytochemistry. Tau. arg and IBE5 could decrease a ~SMA and MMP-7 expression and no influence to MMP-9. IFN had a significantly inhibit: role on a-SMA, MMP-7 fn MMP-9. By above tests.it was believed that 1. continue exist of myofibroblast is a key factor of pulmonary fibrosis. 2. MMP-7 was involved in pulmonary construct break and rebuilding. 3. inflammation is not the mainly cause of pulmonary fibrosis but a complimentary sign. Fb and SMC continuously prol i feration and rebuilding of lung tissue are the mainly cause.1. Tau and arg can descend the content of pulmonary fibrosis by inhibiting Fb proliferation and decreasing MMP-7 secretion. 5. IBE5 can effectly prevent and treatment pulmonary fibrosis by inhibiting Fb activity, proliferation, decreasing Fb transformation toward to myofibroblast, inhibiting MMP-7 expression in lung tissue, interrupting Fb and SMC continuously proliferation and rebuilding of lung tissue construction.2. Preventive and treating mechanism of lung fibrosis using INF including 1) inhibiting Fb activity, proliferation, decreasing Fb transforming to MFb, inhibiting collagen synthesis in activated myofibroblasts. 2)inhibitin...
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