FIGURE 1.

CKI attenuates chronic liver fibrosis. (A) Scheme of experimental procedure for C57BL/6 mice intraperitoneally treated with 4 ml/kg CCl₄ in olive oil for 6 weeks. Mice were intraperitoneally administrated with CKI (7.5 ml/kg) for 3 weeks, starting at 3 weeks post initiation of CCl₄ challenge. (B) Serum levels of ALT, AST, and T‐BIL were detected after the final CKI treatment in CCl₄‐treated mice (n = 10). (C) Scheme of experimental procedure for C57BL/6 mice fed with MCD diet for 4 weeks. Mice were intraperitoneally administrated with CKI (7.5 ml/kg) for 2 weeks, starting at 2 weeks post initiation of MCD diet challenge. (D) Serum levels of ALT, AST, and T‐BIL were quantified after the final CKI treatment in MCD diet‐treated mice (n = 8). (E and F) Mice liver sections from CCl₄‐induced or MCD diet‐induced liver fibrosis models were collected for H&E (original magnification 20 × 10, scale bar 110 μm), Sirius Red (original magnification 20 × 10, scale bar 100 μm), Masson staining (original magnification 10 × 10, scale bar 220 μm), and collagen type1 (COL1A, original magnification 10 × 10, scale bar 210 μm) immunostaining after the final CKI treatment (n = 6). (G) Positive Sirius Red (above) or Masson staining (below) area were quantified by ImageJ analysis (n = 6). (H) Ishak fibrosis score of the Sirius Red‐stained liver sections (n = 6). (I and J) mRNA expression of TGF‐β1, COL1A, Fibronectin, and TIMP1 were analyzed by qRT‐PCR in liver tissues from CCl₄‐challenged (n = 9) or MCD diet‐challenged (n = 8) mice. (K and L) Western blot assay for detecting the expression of TGF‐β1, COL1A, Fibronectin, and TIMP1 in liver tissues from CCl₄‐challenged (K) or MCD diet‐challenged (L) mice. Data are presented as means ± SEM. ns, p > 0.05; *p < 0.05; **p < 0.01; ***p < 0.001