Ameliorating liver fibrosis in an animal model using the secretome released from miR-122-transfected adipose-derived stem cells

Figure 3 Determination of antifibrotic effects of MCM in the in vivo model of liver fibrosis. Control mice and thioacetamide (TAA)-treated mice (mouse model of liver fibrosis) were intravenously (using tail vein) infused with normal saline, CM, and MCM. A, B: Sirius red A and Masson’s trichrome B stains showing that MCM infusion significantly decreased the collagen content of the liver in the mouse model of liver fibrosis. Magnification × 400. Percentages of fibrotic areas were measured using NIH image J and expressed as relative values to those in normal livers; C: Western blot analysis of liver specimens. MCM infusion significantly increased the expression of PCNA (a proliferation marker), and significantly decreased the expression of α-SMA, TGF-β1, and MMP1 (fibrotic markers) and increased an antifibrotic marker (TIMP-1) in the mouse model of liver fibrosis. The relative densities of individual markers had been quantified using Image Lab 3.0 (Bio-Rad) software and then were normalized to that of β-actin in each group. Values are presented as mean ± standard deviation of three independent experiments. ^aP < 0.05 vs Ct (TAA). ^cP < 0.05 between TAA + NCM and TAA + MCM. α-SMA: Alpha-smooth muscle actin; Ct: Control; CM: The secretome obtained from ASCs after 48-h-incubation; MCM: The secretome released from miR-122-transfected ASCs; MMP-1: Metalloproteinases-1; PCNA: Proliferating cell nuclear antigen; TAA: Thioacetamide; TGF-β: Transforming growth factor-β; TIMP-1: Tissue inhibitor of metalloproteinases-1.