Fig. 2: In the BAPN and AngII-induced AAD model, inhibiting intestinal FXR activation can mitigate development and progression of AAD.

A–D Three-week-old male mice were administered with 0.25% BAPN for 30 days with or without UDCA (50 mg/kg/d) and then infused with saline or angiotensin II (1000 ng/kg/min) for 3 days. A Representative morphology of the aortas from different groups of mice. B Survival curve and number at risk (log-rank test). C Incidence of AAD in different groups of mice. (n = 40; chi-square test). D qRT-PCR was performed to validate FXR activation in mouse liver tissue. (n = 6, per group). E The activation status of FXR in mouse intestine was determined by qRT-PCR. (n = 6, per group). F–H Serum levels of FGF15, MMP2, and MMP9 were measured by ELISA. (n = 10, per group). I HE staining, EVG staining, and Masson staining of the aorta (n = 6 from each group). J Statistical chart of the maximum aortic diameter in mice (n = 6 from each group). K Analysis of elastic fiber degradation. (n = 6, per group) (L–N) Immunohistochemical results of MMP2 and MMP9 and the analysis of immunohistochemical (n = 7 per group). O, P Immunofluorescence results show F4/80 (+) cell rate and the expression of COL1 and FN1 and the quantitative analysis. F4/80 (red) in aortas. COL1 (red) in aortas. FN1 (red) in aortas. Nuclei were counterstained with DAPI (blue). (n = 7 per group). Q Hepatic function analysis was performed in mice, and the results are presented. (n = 8, per group). Data in (D–H, J, K, M, N, P,Q) are shown as the mean ± SEM. Statistical analysis was performed using a one-way anova test with Dunnett’s multiple comparisons posttest. (*p < 0.05, **p < 0.01, ***p < 0.001). Scale bars: 200 μm and 50 μm.