Preventive effect of interferon-γ of Chinese genotype on radiation pulmonary fibrosis
Tao Liu
Abstract
Tao Liu
Abstract
Objective To investigate the inhibitive effect of Interferon-γ (γ-IFN) of Chinese genotype on proliferation of human lung fibroblast (HLF) induced by radiation, and examine its possible mechanism and role in prevention and treatment of radiation pulmonary fibrosis. Methods The proliferation of HLF was determined by MTT assay, the expression of γ-smooth muscle actin (α-SMA) and the synthesis of collagen type IV by immunocytochemistry assays. Results Chinese α-IFN was observed to inhibit, proportionally to irradiation dose, the proliferation of HLF induced by 60Co γ-irradiation. The expression of α-SMA was remarkable in cytoplasmic matric after the irradiation, suggesting that irradiation could induce the transformation from fibroblast (FB) to myofibroblast (MFB). The expression of collagen Ⅳ was increased with irradiation. Compared with the irradiated group, the expression of collagen IV was lower when γ-IFN was administered before being irradiated.Conclusion 60Co γ irradiation can induce pulmonary fibrosis by promoting the proliferation of HLF, inducing the transformation from FB to MFB, and increasing the excreting of collagen type Ⅳ.γ-IFN can prevent pulmonary fibrosis by effectively inhibiting the abnormal proliferation of HLF and the excessive synthesis of collagen Ⅳ after irradiation.;
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Objective To investigate the inhibitive effect of Interferon-γ (γ-IFN) of Chinese genotype on proliferation of human lung fibroblast (HLF) induced by radiation, and examine its possible mechanism and role in prevention and treatment of radiation pulmonary fibrosis. Methods The proliferation of HLF was determined by MTT assay, the expression of γ-smooth muscle actin (α-SMA) and the synthesis of collagen type IV by immunocytochemistry assays. Results Chinese α-IFN was observed to inhibit, proportionally to irradiation dose, the proliferation of HLF induced by 60Co γ-irradiation. The expression of α-SMA was remarkable in cytoplasmic matric after the irradiation, suggesting that irradiation could induce the transformation from fibroblast (FB) to myofibroblast (MFB). The expression of collagen Ⅳ was increased with irradiation. Compared with the irradiated group, the expression of collagen IV was lower when γ-IFN was administered before being irradiated.Conclusion 60Co γ irradiation can induce pulmonary fibrosis by promoting the proliferation of HLF, inducing the transformation from FB to MFB, and increasing the excreting of collagen type Ⅳ.γ-IFN can prevent pulmonary fibrosis by effectively inhibiting the abnormal proliferation of HLF and the excessive synthesis of collagen Ⅳ after irradiation.;
Key concepts: Pulmonary fibrosis, Fibroblast, Myofibroblast, Fibrosis, Chemistry, Irradiation, Immunocytochemistry, Cell growth