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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