Figure 3
From: TGF-β-induced hepatocyte lincRNA-p21 contributes to liver fibrosis in mice
Ectopic expression of miR-30b in hepatocyte suppresses CCl4-induced liver fibrosis. Mice were treated with oil (Sham, n = 6), CCl4 (CCl4, n = 6), CCl4 in combination with injection of AdH-NC (CCl4 + AdH-NC, n = 6) and CCl4 in combination with injection of AdH-miR-30 (CCl4 + AdH-miR-30, n = 6). The mice were sacrificed after 3 weeks CCl4 treatment. (A) Liver fibrosis was evaluated by H&E staining (100×), sirius red staining (40×), α-SMA immunofluorescence staining (100×) and collagen I immunohistochemical staining (100×). (B) Quantifications of the sirius red positive area and hepatic hydroxyproline content. The hydroxyproline contents are expressed as μg/g wet liver weight. (C) Hepatic Collagen I, TIMP-1 and TGF-β1 mRNA were determined by qRT-PCR. (D) miR-30b level in the whole liver, isolated hepatocytes and HSCs were determined by qRT-PCR respectively. (E) Immunofluorescence staining of liver sections with anti-F4/80 antibody. Scale bar, 50 μm. (F) Hepatic IL-6, IL-1β and CCL2 mRNA were determined by qRT-PCR. The results are shown as fold change compared with Sham group or AdH-NC group mice. Data are the mean ± SEM of three independent experiments. *P < 0.05, **P < 0.01. NS, no significant change.
