Figure 4
From: TGF-β-induced hepatocyte lincRNA-p21 contributes to liver fibrosis in mice
Knockdown of lincRNA-p21 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-shNC (CCl4 + AdH-shNC, n = 6) and CCl4 in combination with injection of AdH-shlincp21 (CCl4 + AdH-shlincp21, 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 α-SMA, collagen I, TGF-β1, TIMP-1 and CTGF mRNA were determined by qRT-PCR. (D) Hepatic IL-6, IL-1β and CCL2 mRNA were determined by qRT-PCR. (E) lincRNA-p21 levels in the whole liver, hepatocytes and HSCs were determined by qRT-PCR respectively. (F) miR-30 levels in the isolated hepatocytes were determined by qRT-PCR. The results are shown as fold change compared with Sham group or AdH-shNC group mice. Data are the mean ± SEM of three independent experiments. *P < 0.05, **P < 0.01. NS, no significant change.
