Figure 5
From: TGF-β-induced hepatocyte lincRNA-p21 contributes to liver fibrosis in mice
Inhibition of miR-30 impairs the effects of lincRNA-p21 knockdown on CCl4-induced liver fibrosis. Mice were treated with oil (Sham, n = 6), CCl4 (CCl4, n = 6), CCl4 in combination with injection of AdH-shlincp21 and SCR (AdH-shlincp21 + SCR, n = 6) and CCl4 in combination with injection of AdH-shlincp21 and anti-miR-30 (AdH-shlincp21 + anti-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 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 and F) lincRNA-p21 and miR-30b levels in the isolated hepatocytes were determined by qRT-PCR respectively. The results are shown as fold change compared with Sham group mice. Data are the mean ± SEM of three independent experiments. *P < 0.05, **P < 0.01.
