Fig. 2
Knockdown of lnc-Helf alleviates hepatic fibrosis induced by CCl4. Mice were divided into six groups: AAV8-NC, NC + CCl4, lnc-Helf-sh1#, lnc-Helf-sh1# + CCl4, lnc-Helf-sh2#, and lnc-Helf-sh2# + CCl4. Mice were injected with AAV8-lnc-Helf-shRNAs, or AAV8-NC virus 2 weeks after the first injection of CCl4 via tail vein. After CCl4 treatment for 8 weeks. A qRT–PCR was used to assess the expression of lnc-Helf in livers of each group (n = 3). B The significantly differentially expressed mRNAs were displayed by hierarchical cluster analysis: bright red, upregulation; bright blue, downregulation (n = 3). C–E The Venn diagram, KEGG, and GO analyses of differentially expressed mRNAs in lnc-Helf-sh1# + CCl4 mice and lnc-Helf-sh2# + CCl4 mice, compared with NC + CCl4 mice. F The degree of liver fibrosis was evaluated by morphological detection: H&E staining, Masson staining, Sirius red staining, and IHC for α-SMA; five images of each liver and five livers from different mice were quantified for each group; scale bar is 100 μm for 40× and 400 μm for 10× magnifications . G Western blot was used to determine the protein level of MMP2, α-SMA, and TIMP1. GAPDH was used as an internal control. H The content of hepatic hydroxyproline was quantified in livers of each group (n = 5). The data were displayed as hydroxyproline (μg)/liver wet weight. Data are presented as mean ± SEM. */#p < 0.05. *p < 0.05 for AAV8-NC. #p < 0.05 for NC + CCl4, one-way ANOVA (A, F, H)