FBP1 as a key regulator of focal adhesion kinase-mediated hepatic stellate cell activation: Multi-omics and experimental validation

Figure 4 In mouse models of liver fibrosis, focal adhesion kinase inhibition ameliorates hepatic fibrosis. A: Liver tissues from mice in each group were stained with hematoxylin and eosin (HE) to observe inflammatory cell infiltration, cellular morphology, and lobular architecture; Masson’s trichrome staining and Sirius red staining were performed to assess fiber deposition; B: Immunohistochemical analysis was conducted to detect the expression of fructose-1,6-bisphosphatase 1 (FBP1) protein in the livers of mice from each group, and the number of positive cells in each group was statistically analyzed. Scale bar: 200 μm, 50 μm; C: Western blot (WB) analysis was used to detect the expression of liver fibrosis marker alpha smooth muscle actin (α-SMA), as well as focal adhesion kinase (FAK) and phosphorylated FAK (p-FAK) proteins, with β-actin as the internal control; D: Grayscale value analysis was performed, and statistical significance relative to the normal group or carbon tetrachloride (CCl₄) group was assessed; E: WB analysis was employed to detect the protein expression of aerobic glycolysis enzymes, including lactate dehydrogenase A (LDHA), hexokinase 2 (HK2), phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3), pyruvate kinase M2 (PKM2), and FBP1, with β-actin as the internal control; F: Grayscale value analysis was conducted, and statistical significance relative to the normal group or CCl₄ group was evaluated. All data are from three independent samples. Data are represented as the mean ± SD. ^aNot significant; ^bP < 0.01, ^cP < 0.001, ^dP < 0.0001.