Fig. 6

Amelioration of UGT mediated bile acid disorder by activating FXR-Sirt1-LKB1-P53 axis in mice. A Mice were randomly assigned to one of the four groups shown in (A), except from control group, treated with oral gavage with saline or FXR agonist, or injection with LKB1 inhibitor, subsequently these mice received 3% DSS daily drink. B Body weight changes (n = 6). C Total bile acid concentration in the feces (n = 6). D UGT1A4 enzyme content in the colon (n = 6). E Histomorphology score (n = 6). Scale bars, 200 μm. F, G Intensity of FXR and LKB1 in the colon were showed by Immunohistochemistry (n = 3).Scale bars, 50 μm. (H) TUNEL⁺ cell in the colon was counted (n = 3). Scale bars, 20 μm. The differences between groups were compared using either student’s t-test or two-way analysis of variance (ANOVA) followed by Tukey’s test for multiple comparisons, and statistical significance was considered at P < 0.05. Data were represented as mean ± SEM, and exhibited *P < 0.05, **P < 0.01, ***P < 0.001