Fig. 3

The central role of LKB1 activated by FXR in anti-apoptosis and BA disorder diarrhea. A Isolation of primary gut epithelial cells from healthy and BADD piglets for transcriptomic sequencing. B Nucleus location of FXR analyzed by immunofluorescence. Scale bars, 50 μm. C Significant differential genes enriched in gut epithelial cells (n = 3–7). D Relative gene level of LKB1 in response to FXR activation (n = 3). E LKB1 level is analyzed from GSE14842 (n = 4–5). F, G Relative protein expressions of FXR, LKB1, BCL2, and BAX after FXR activation in the inflammatory situation (n = 3). H, I Relative protein expressions of FXR, LKB1, and BAX in the treatment of FXR siRNA (n = 3). J, K Relative protein expressions of FXR, LKB1, and BAX in the treatment of LKB1 siRNA (n = 3). 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