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Investigations of Molecular Mechanism and Protection on Radiation Pulmonary Fibrosis

Author: HuangShanYing
Tutor: SongLiangWen
School: PLA Military Academy of Medical Sciences
Course: Pathology
Keywords: CTGF Fibroblasts Radiation-induced lung injury Reconstruction Pulmonary fibrosis
CLC: R818
Type: Master's thesis
Year: 2005
Downloads: 143
Quote: 1
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Abstract


Purpose and significance: the radiation-induced lung fibrosis (radiation pulmonary fibrosis, RPF) is the end stage of lung tissue subjected to radiation injury secondary alveolar structure caused by invalid reconstruction, the detailed molecular mechanism has not yet been completely elucidated. Connective tissue growth factor (CTGF) is a newly discovered fibrogenic growth factors, may play a crucial role in the process of pulmonary fibrosis. This paper through the study of the onset of action of CTGF RPF CTGF expression and into fiber cell activation, proliferation and transformation between the role of relationship and Col Ⅳ Their degrading enzymes MMP-9 in the alveolar tissue reconstruction, to explore the molecular mechanisms of pulmonary fibrosis, while observing the gamma-interferon (IFN-gamma) on the prevention and treatment of pulmonary fibrosis. This study reveals the pathogenesis of radiation-induced lung fibrosis, early and effective prevention and treatment of pulmonary fibrosis in the development of great significance. Materials and Methods: cells in vitro and in vivo animal to establish 60 Coγ-ray-induced radiation-induced lung fibrosis model, and then with different doses of TGF-beta1 and IFN-gamma-treated cells, the use of conventional and special staining study the morphological changes of the radiation-induced lung fibrosis; immunohistochemistry and Western blot CTGF and its related factors such as alpha-SMA, MMP-7, MMP-9, Col IV of expression; using MTT, Hoechst staining and flow cytometry detection of irradiation, TGF-beta1 and IFN-gamma RLF biological effects and cell cycle changes. Results: (1) Cell Experimental results show that a certain dose of 60 Co gamma-ray irradiation to promote cultured rat lung fibroblasts (RLF) proliferation, 6-24 hours after irradiation of cells in S phase increased ,24-48 G2-M phase cells increased, and through the expression of alpha-SMA occurrence of phenotypic changes, transformed into myofibroblasts (MFB). (2) RLF activation, CTGF gene expression increased CTGF protein synthesis, synthetic Col IV, MMP-7 and MMP-9 also increased. (3) TGF-β1 can promote the the RLF proliferation and phenotypic changes and induction of CTGF gene expression and protein, showing a dose-effect relationship, (4) the irradiated lung tissue of rats experienced exudative, proliferative phase, fiber of the period, I, III, type IV collagen synthesis, fibrosis. CTGF, MMP-7, MMP-9 in pulmonary fibrosis in different periods of high expression to participate in the ongoing reconstruction process of the alveolar tissue. (5) IFN-gamma can inhibit the RLF into S phase, resulting in G 1 of block and inhibit proliferation and induce apoptosis RLF; decrease of CTGF, Col Ⅳ and MMP-9 generation and fibroblasts The phenotypic changes. Conclusions: (1) CTGF is a key growth factor for the radiation-induced lung fibrosis. It can promote the activation of fibroblasts proliferation, a change in phenotype and cytokine production, and promoting ECM mediated through the TGF-beta

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CLC: > Medicine, health > Of Medical > Radiation Medicine > Radiation sickness,radiation damage
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