Relaxin attenuates silica-induced pulmonary fibrosis by regulating collagen type I and MMP-2.

Silicosis is one of the most prevalent occupational lung diseases, but the pathogenic mechanisms of silicosis are largely unknown and an effective treatment is not yet available. In this study, we investigated the potential effects of relaxin (RLX) on fibrosis by an in vitro model involving silica-induced and macrophage-mediated pulmonary fibroblasts. Following pre-treatment with DQ12 quartz, the culture supernatant of human monocytic THP-1 cells was added to human fetal lung fibroblast MRC-5 cells with or without RLX. DQ12 significantly induced an increase of TGFB1 mRNA in THP-1 cells, coinciding with elevated TGF-β1 protein excretion in the supernatant, but RLX had no effect on DQ12-stimulated TGF-β1 secretion in THP-1 cells. Furthermore, RLX inhibited the proliferation of MRC-5 cells, and reduced the mRNA level and protein secretion of collagen type I, whereas it increased the mRNA level and protein activity of MMP-2 in MRC-5 cells treated with THP-1 cell culture supernatant. Our data suggest that RLX may inhibit TGF-β1-mediated fibrosis during the process of silicosis, providing evidence for the protective effect of RLX on silica-induced pulmonary fibrosis.