Fig. 5

RvD1 suppressed the expression of COMP, FOXM1 and ROS level mediated by ALX/FPR2. (a) The expression of ALX/FPR2, one of RvD1receptor, in HCC tissues was significantly lower than that in normal liver tissues, while the expression of GPR32 was no significant difference. Data from a database named R2: Genomics Analysis and Visualization Platform (http://r2.amc.nl). **P < 0.01by t test. (b) The expression of ALX/FPR2 and GPR32 in CAFs isolated from five HCC patients were determined by western blotting. * P < 0.05 or ** P < 0.01 by t test. (c) CAFs were transfected with siRNA targeting ALX/FPR2 (si-FPR2) or negative control (si-NC), and 24 h later, 400 nM RvD1 or vehicle were utilized to treat these cells for 48 h. Then ALX/FPR2, α-SMA, COMP and FOXM1 were detected by western blotting. n = three independent experiments, ** P < 0.01 by ANOVA. (d) CAFs were transfected with siRNA targeting ALX/FPR2 (si-FPR2) or negative control (si-NC), and 24 h later, 400 nM RvD1 or vehicle were utilized to treat these cells 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. (e-f) CAFs were transfected with si-FPR2 then treated with RvD1, and the intracellular ROS level was determined by immunofluorescence analysis and flow cytometry analysis using DCF-DA probe. Magnification is × 400, and scale bars = 20 μm. n = three independent experiments, ** P < 0.01 by ANOVA