Fig. 6.

CHP recovers liver fibrosis and inflammation in a therapeutic protocol.

(A) Animal study flow. Mice received 6 injections of CCl₄ over 13 days and were treated with CHP daily starting after the third CCl₄ injection. Liver and plasma were collected at Day 14. (B, C) ALT (B), and AST (C) plasma levels. Whiskers in boxplots represent the minimum to maximum range. (D) Liver expression of genes involved in fibrosis and inflammation. Error bars in bar plots represent the standard deviations. (E) Western blotting of αSMA expression; vinculin was used as loading control. (F) Quantification of αSMA signals from the western blotting in (E), normalised on vinculin. Error bars in bar plots represent the standard deviations. (G) Western blotting of fibronectin expression; vinculin was used as the loading control. (H) Quantification of fibronectin signal from the western blotting in (G), normalised on vinculin. Error bars in bar plots represent the standard deviations. (I) Representative images of liver sections stained with H&E or Sirius Red (0.1% Direct Red and 0.1% Fast Green FCF) (n = 2 for CTRL, n = 6–7 for other treatments). One-way ANOVA, followed by Dunnett’s multiple comparison test vs. CCl₄ group was used for statistical analysis (B-D, F, H). ∗p <0.05; ∗∗p <0.01; ∗∗∗p, <0.001; ∗∗∗∗p <0.0001. ALT, alanine transaminase; AST, aspartate transaminase; CCl₄, carbon tetrachloride; CHP, cyclo(His-Pro); CTRL, control; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; IL-6, interleukin 6; αSMA, alpha smooth muscle actin; TNF-α, tumour necrosis factor alpha.