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本研究结合体内外实验,探讨了钙结合蛋白S100A8在放射性肺纤维化早期的表达及意义。20Gy60Coγ射线全胸照射大鼠,建立大鼠放射性肺纤维化模型,分别于照射后1周、2周及4周活杀后取肺,采用免疫组化方法检测S100A8蛋白水平的变化;采用RT-PCR方法检测S100A8及与其形成复合物的S100A9 mRNA水平的变化。对于体外培养的小鼠巨噬细胞RAW264.7,采用RT-PCR方法检测该细胞受γ射线与脂多糖(Lipopolysaccharides,LPS)处理后S100A8 mRNA水平的变化。照射后4周,S100A8蛋白在大鼠肺部巨噬细胞胞浆增强表达,S100A8和S100A9 mRNA在大鼠肺部也增强表达。结果表明,RAW264.7细胞中,γ射线与LPS能够协同作用增强该细胞S100A8 mRNA的表达。S100A8在放射性肺纤维化早期于巨噬细胞表达增强,发挥其趋化活性,参与炎症发生,进而在放射性肺纤维化形成过程中发挥作用。
In this study, in vitro and in vivo experiments to explore the calcium binding protein S100A8 in the early stage of radiation-induced pulmonary fibrosis and its significance. Whole lungs were irradiated with 20Gy60Coγ-ray to establish the model of radiation-induced pulmonary fibrosis in rats. The lungs were killed and killed at 1, 2 and 4 weeks after irradiation. The expression of S100A8 protein was detected by immunohistochemistry. PCR method was used to detect the change of S100A8 mRNA level and the S100A9 mRNA level. For mouse macrophage RAW264.7 cells cultured in vitro, the changes of S100A8 mRNA level after treatment with γ-rays and lipopolysaccharides (LPS) were detected by RT-PCR. Four weeks after irradiation, S100A8 protein was enhanced in the cytoplasm of rat lung macrophages, and S100A8 and S100A9 mRNAs were also enhanced in the lungs of rats. The results showed that, in RAW264.7 cells, γ-rays and LPS can synergistically enhance the expression of S100A8 mRNA in the cells. S100A8 enhances the expression of macrophages in early stages of radiation-induced pulmonary fibrosis, exerts its chemotactic activity, participates in inflammation, and plays a role in the formation of radiation-induced pulmonary fibrosis.