Fig. 2: Hepatocyte MCM7 knockdown attenuates liver fibrosis in S. japonicum-induced mice.

A Experimental design schematic: mice were infected with S. japonicum and received intravenous injections of either shCtrl or AAV-shMcm7 on day 10 post-infection. Liver samples were collected at 8 weeks post-infection for analysis. B H&E staining (areas positive for liver fibrosis are delineated by black dashed lines), Masson’s trichrome staining, COL1A1 staining, and α-SMA staining (all scale bars: 100 μm) of liver sections from the indicated groups (AAV-shCtrl/uninfected, AAV-shMcm7/uninfected, AAV-shCtrl/infected, AAV-shMcm7/infected). Graphs show the quantified positive areas for each stain, determined using ImageJ software from multiple randomly selected fields across distinct tissue sections. C Hydroxyproline content in liver tissues was determined. D The size of the granuloma area in S. japonicum-induced mice (AAV-shCtrl/infected, AAV-shMcm7/infected) was measured and calculated. E, F qRT-PCR (E) was used to assess the expression levels of Col1a1, α-Sma, Timp1, and Mmp2, while Western blot (F) analysis focused on COL1A1 and α-SMA in liver tissues from the indicated groups, with the graph displaying protein levels. Data are presented as the mean ± SD of 3–6 mice per group and are representative of three independent experiments. Statistical analyses were performed using an unpaired Student’s t-test or one-way ANOVA. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001; ns not significant.