Fig. 3.

RvD1 abolishes secretion of COMP, down-regulates ROS level and suppresses FOXM1 expression in CAFs. (a) CAFs were treated with RvD1 (0, 200, 400 and 800 nM) for 24 h, then serum-starved for an additional 48 h, and the CAFs culture media was used to detect the secretion of COMP by Elisa assay. n = three independent experiments, **P < 0.01 by ANOVA. (b) CAFs were administrated with RvD1 (0, 200,400 and 800 nM) for 48 h, western blotting was used to detect the expression of Col 1α1, Col 3α1, α-SMA, fibronectin, HAS2, CTGF, COMP, MMP2 and FOXM1. n = three independent experiments, **P < 0.01 by ANOVA. (c) The migration capacity of CAFs in response to RvD1 (400 nM) was detected by Transwell-migration assay. Magnification is × 100, and scale bars = 50 μm. n = three independent experiments, **P < 0.01 by t test. (d) CAFs were administrated with RvD1(0, 400 nM) for 24 h, the expression of Col 1α1, Col 3α1, α-SMA, fibronectin, HAS2, CTGF, COMP, MMP2 and FOXM1 at mRNA level were assessed by qRT-PCR. n = three independent experiments, **P < 0.01 by t test. (e and f) CAFs were treated with RvD1, and the intracellular ROS level was determined by immunofluorescence analysis and flow cytometry using DCF-DA probe. Magnification is × 400, and scale bars = 20 μm. n = three independent experiments, **P < 0.01 versus control by t test