| Objective Radiation pulmonary fibrosis(RPF) is the end phase of pulmonary ineffective reconstruct after irradiation and its mechanism is still unclear. CTGF is a newly described 38-kDa peptide mitogen for fibroblasts and play an important role on development of RPF. This experiment was performed to explore the effect of CTGF in the initiation of RPF and the relation to activation, proliferation of fibroblasts, role of collegen IV and MMP-7,9 on reconstruct of pulmonary alveolus, as well as preventive effect of IFN-γ on RPF. Therefore this study possesses not only a profound theoretical value on exploring the pathogenesis of RPF, but also an instructive significance on early effective prevention and treatment of RPF as well.Materials and methods This experiment was performed in two levels including cells and animals. Cell and animal model were replicated by 60Co y-ray and then different doses of TGF-β1 and IFN-γ were administrated to RLF. Morphological and collagen I and III in lungs were observed or determined by HE, Sirius red staining and polarization microscope; Expression of CTGF, α-SMA, MMP-7, MMP-9 and collegen IV were detected by Western blot page, immunohistochemistry and illustration analysis; Cellular biological effect and cellcycle alteration caused by irradiation, effect of TGF-β1 and IFN-γ on RLF were determined by MTT colorimetry, flow cytometry and hoechst staining.Results (l)The result of cellular experiment displayed that irradiation could promote activation and proliferation of Fibroblast(Fb) and transformation to myofibroblast(MFb) by phenotype; the rate of cellular S phase increased during 24h and the rate of G2-M phase increased during 24-48h after 60Co y-ray irradiation. (2) 60Co y-ray irradiation increased expression of mRNA and synthesis of proteins of CTGF, Col IV, MMP-7, MMP-9 in RLF. (3) TGF-β1 could promote activation, proliferation of RLF and up-regulate CTGF expression in vitro. (4) Pathologically alterations displayed effusion,... |
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