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. 2020 Jul 9;9(1):1785738. doi: 10.1080/20013078.2020.1785738

Figure 5.

Figure 5.

Sja-miR-71a inhibits HSCs activation to alleviate liver fibrosis by inhibiting Sema4D. (a). The co-localization of GFAP and Sema4D in liver sections was observed, DAPI was used as a counterstain. (b). Expression level of Sema4D was determined by western blotting for LX2 cells treated with PBS, TGF-β1 and TGF-β1+ Sja-miR-71a mimic. (c). The co-localization of α-SMA and Sema4D in liver sections was observed, DAPI was used as a counterstain. (d). The co-localization of α-SMA and Sema4D in LX2 cells (treated with PBS, TGF-β1 and TGF-β1+ Sja-miR-71a mimic) was observed, DAPI was used as a counterstain. (e, f). LX2 cells treated with PBS, TGF-β1, Recombinant Human Sema4D, Recombinant Human Sema4D+Sja-miR-71a mimic, Recombinant Human Sema4D+TGF-β1, Human Plexin B1 siRNA+TGF-β1 and Human CD72 siRNA+TGF-β1 for 48 h. Expression levels of α-SMA and Collagen I were determined by qRT-PCR (n = 5 per group) and western blotting (n = 4 per group). Results are shown as mean ± SD. One-way ANOVA test was used for statistical analysis.