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Fig. 3 | BMC Medicine

Fig. 3

From: LncRNA Airn maintains LSEC differentiation to alleviate liver fibrosis via the KLF2-eNOS-sGC pathway

Fig. 3

Over-expression of Airn alleviated CCl4-induced liver fibrosis in vivo. Mice were divided into four groups: AAV8-GFP (n = 10), AAV8-GFP + CCl4 (n = 10), AAV8-Airn (n = 10), and AAV8-Airn + CCl4 (n = 10), and transduced with AAV8-GFP or AAV8-Airn virus via tail vein 2 weeks after the first injection of CCl4, after 8 weeks of CCl4 treatment. A The expression of Airn in livers of each group was examined by qRT-PCR. B Liver fibrosis was evaluated by macroscopic examination, H&E staining, sirius red staining, and IHC for α-SMA, COL1α1, and PCNA; scale bar, 400 μm for 10× and 100 μm for 40×. Right, five images of each liver and five livers from different mice were quantified for each group. C The protein level of α-SMA, COL1α1, MMP2, and TIMP1 was determined by western blot and quantitatively compared with GAPDH as a reference control. D The mRNA level of α-SMA, Col1α1, Mmp2, and Timp1, and Cd31 and Laminin was determined by qRT-PCR. E Liver sections from CCl4-induced fibrotic liver were analyzed using SEM and the protein level of CD31 and LAMININ was detected by IHC staining and quantitatively compared; scale bar, 400 μm for 10× and 100 μm for 40×. *p<0.05 stands for AAV8-GFP+CCl4 or AAV8-Airn vs AAV8-GFP. #p<0.05 stands for AAV8-Airn+CCl4 vs AAV8-GFP+CCl4

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