Mechanism of annexin A1/N-formylpeptide receptor regulation of macrophage function to inhibit hepatic stellate cell activation through Wnt/β-catenin pathway

Figure 1 Annexin A1 inhibited CCl₄-induced liver injury. A: Gross view of liver tissue. The liver of mice in the control group was red with bright color and smooth surface. In the CCl₄-induced model group, the liver was light in color, rough and grainy on the surface. Liver tissue nodules appeared at 8 wk, and fibrosis appeared at 8 wk in Anxa1^-/- mice. After Ac2-26 treatment, the liver was mostly dark red, and the surface roughness was reduced. The effect of Ac2-26 was reversed by Boc2, and the liver color became lighter, the surface was grainy, the edge was blunt, and the texture was hard; B: Annexin (Anx)A1 was expressed in liver tissue. Anxa1 was stained brown. Compared with the control group, the liver tissue in mice treated with CCl₄ showed obvious AnxA1 staining. More liver tissue was stained at 8 wk than at 4 wk. The AnxA1^-/- model groups were hardly stained. More tissue staining was observed in the CCl₄-induced model group after Ac2-26 treatment, while staining was almost absent after Boc2 intervention; C: AnxA1 mRNA expression; D: Protein expression of AnxA1, α-smooth muscle actin, β-catenin, and GAPDH (n = 8). Results are presented as ratios of target mRNA or protein normalized to internal GAPDH. ^aP < 0.05 vs control; ^bP < 0.01 vs CCl₄; ^cP < 0.05 vs CCl₄ + Ac2-26; ^dP < 0.05 vs intra-group. Ac2-26: Active N-terminal peptide of annexin A1; AnxA1: Annexin A1; Boc2: N-formyl peptide receptor antagonist N-Boc-Phe-Leu-Phe-Leu-Phe; α-SMA: α-smooth muscle actin.