李小峰, 廖静, 鲁文清, 刘爱林. 松弛素在大鼠矽肺形成过程中肺组织的表达及作用[J]. 环境与职业医学, 2012, 29(3): 132-135.
引用本文: 李小峰, 廖静, 鲁文清, 刘爱林. 松弛素在大鼠矽肺形成过程中肺组织的表达及作用[J]. 环境与职业医学, 2012, 29(3): 132-135.
LI Xiao-feng , LIAO Jing , LU Wen-qing , LIU Ai-lin . Expression and Potential Role of Relaxin in Lung Tissue of Rats Developing Silicosis[J]. Journal of Environmental and Occupational Medicine, 2012, 29(3): 132-135.
Citation: LI Xiao-feng , LIAO Jing , LU Wen-qing , LIU Ai-lin . Expression and Potential Role of Relaxin in Lung Tissue of Rats Developing Silicosis[J]. Journal of Environmental and Occupational Medicine, 2012, 29(3): 132-135.

松弛素在大鼠矽肺形成过程中肺组织的表达及作用

Expression and Potential Role of Relaxin in Lung Tissue of Rats Developing Silicosis

  • 摘要: 目的 探讨松弛素(relaxin)在石英尘诱导矽肺形成中的潜在作用。

    方法 建立矽肺体内动物模型和体外细胞模型,在动物模型中应用免疫组织化学法和实时荧光定量PCR分析肺组织松弛素蛋白及基因表达,在细胞模型中通过酶联免疫法测人胚肺成纤维细胞(HFL-Ⅰ)Ⅰ型胶原分泌量。

    结果 松弛素蛋白在大鼠正常肺组织中弱表达,主要定位于Ⅰ型肺泡细胞。大鼠染石英尘(DQ12)后肺组织松弛素蛋白和mRNA表达呈现先上升后下降的趋势,主要定位于Ⅰ型肺泡细胞和巨噬细胞;与对照组相比,染石英尘后第7天松弛素蛋白水平达到最高(P<0.05),第14天时无明显差异(P>0.05),第28天时明显减少(P<0.05)。与DQ12组相比,松弛素处理组中HFL-Ⅰ细胞Ⅰ型胶原的生成明显减少(P<0.05)。

    结论 松弛素可以抑制石英尘诱导的肺成纤维细胞胶原合成,可能对石英尘诱导矽肺发生有影响。

     

    Abstract: Objective To investigate the potential role of relaxin in the development of silica-induced silicosis.

    Methods Both in vitro and in vivo models of silicosis were established. Relaxin gene and protein expression in rat lung tissues were determined by real-time quantitative polymerase chain reaction (PCR) and immunohistochemical staining, respectively. Type I collagen in human fetal lung fibroblasts (HFL-I) supernatants was measured by enzyme-linked immunosorbent assay (ELISA).

    Results Slight expression of relaxin was observed in the normal control rat lung tissues and the signal intensities were primarily located in pulmonary alveolar type I cells. The relaxin protein and gene expression in the lungs of silica-treated (Dorentrup quartz, DQ12) rats showed a tendency of increasing first and then decreasing and was primarily located in pulmonary alveolar macrophages and type I cells. Compared with the controls, the relaxin protein expression reached maximum at 7 d (P<0.05), then went down at 14 d (P>0.05), and decreased markedly at 28 d (P<0.05). The levels of type I collagen in HFL-I cells in the relaxin group was significantly lower than that in the DQ12 group (P<0.05).

    Conclusion Relaxin can inhabit the formation of silica-induced type I collagen in lung fibroblasts, which may affect the development of silica-induced silicosis.

     

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