Fig. 5. Periostin is implicated in the development of liver fibrosis in mice.

A Schematic overview illustrating the construction process of the CCl₄-induced liver fibrosis model in WT and Periostin knockout (Periostin KO) mice (n = 6 per group). B, C Serum levels of ALT and AST, as well as the protein levels of Periostin, Col-I, and α-SMA in liver tissues, were measured in the indicated groups. D H&E, Sirius red, and α-SMA staining demonstrated that the absence of Periostin mitigated liver fibrosis in murine models induced by CCl₄. The data were quantified (n = 6 per group) (Scale bar: 50 μm). E Western blot analyses indicated decreased levels of CCNE1, PCNA, and α-SMA in primary HSCs isolated from Periostin KO mice treated with CCl₄. F Schematic overview illustrating the experimental strategy of administering recombinant Periostin-His tagged protein (rPeriostin) in CCl₄-induced αSMA-TK mice treated with GCV (n = 6 per group). G Immunofluorescence staining demonstrated the rPeriostin (red) were internalized by the elevated population of aHSCs (green) in the liver of αSMA-TK mice treated with rPeriostin (Scale bar: 50 μm). H Serum ALT and AST levels were measured in indicated groups. I H&E and Sirius red staining in liver sections of αSMA-TK mice from indicated groups. The data were quantified (n = 6 per group) (Scale bar: 50 μm). J Protein expression levels of Periostin, Notch-1, Col-I, and α-SMA in liver tissues from αSMA-TK mice from the indicated groups. K Protein expression levels of Notch-1, PPAR-γ, GFPA, Vim, and α-SMA in rPeriostin treated-primary HSCs (isolated from un-injured WT mice) with or without administration of Notch-1 inhibitor (10 μM). All results are shown as mean ± SEM. *p < 0.05; ***p < 0.001. WT wild type, KO knockout, CCl₄ carbon tetrachloride, ALT alanine aminotransferase, AST aspartate aminotransferase, Col-I Collagen-I, CCNE1 cyclin E1, TK thymidine kinase, GCV ganciclovir, Vim Vimentin.