Fig. 2

hPMSCs improve inflammation microenvironment in CCl₄-induced liver fibrosis. a Immunohistochemistry staining using anti F4/80 antibodies at 2 weeks after the second injection of hPMSCs. b Monocyte-derived macrophage (MoMF) or Kupffer cells (KC) isolated from liver tissues were detected by FCAS analysis. MoMFs (CD11b^highF4/80^low) were inside the black circle and KCs (CD11b^lowF4/80^high) were inside the red circle. c A statistical analysis was performed to determine the proportion of MoMF or KC in CD45+ cells. d Inflammatory cytokines in serum (IL-6, TNF-α, IFN-γ) were examined with ELISA assays. e Expression of inflammatory cytokines mRNA was determined using qRT-PCR. Relative mRNA expression was normalized to β-actin and compared with the fibrosis group. Mice from fibrosis group received CCl₄ followed by PBS injection. Scale bar, 50 μm. ****p < 0.0001, ***p < 0.001, **p < 0.01, *p < 0.05; ns, no significance. Normal and fibrosis mice, n = 5/group; hPMSCs mice, n = 7/group