Calcitriol attenuates liver fibrosis through hepatitis C virus nonstructural protein 3-transactivated protein 1-mediated TGF β1/Smad3 and NF-κB signaling pathways

Figure 1 Evaluation of nonstructural protein 3-transactivated protein 1 expression in carbon tetrachloride-induced hepatic fibrosis and Transforming growth factor 1 beta 1-stimulated LX-2 cells. A: Real-time quantitative polymerase chain reaction analysis of fibrosis-related genes in liver tissues (n = 6); B: Immunofluorescence staining for alpha smooth muscle actin (α-SMA); red: α-SMA (n = 3), scale bar = 20 μm; C: Immunohistochemical staining for α-SMA, scale bar = 100 μm; D: Image J analysis of immunohistochemical staining for α-SMA (n = 3); E: Immunofluorescence staining for nonstructural protein 3-transactivated protein 1 (NS3TP1); green: NS3TP1 (n = 3), scale bar = 20 μm; F: Western blot analysis of NS3TP1 in L02, LX-2, Huh7, and G2 cells; G and H: NS3TP1 was overexpressed in LX-2 cells treated with transforming growth factor 1 beta 1 (TGFβ1) for 24 h (n = 3). The data was presented as mean ± SE. ^aP < 0.05, ^bP < 0.01 vs TGFβ1 (0 ng/mL) group; ^cP < 0.01 vs corn oil control group. NS3TP1: Nonstructural protein 3-transactivated protein 1; TGFβ1: Transforming growth factor 1 beta 1; CCl₄: Carbon tetrachloride; RT-qPCR: Real-time quantitative polymerase chain reaction; α-SMA: Alpha smooth muscle actin.