Fig. 1: The decreased levels of ursodeoxycholic acid in both AAD patients and mouse serum suggest that intestinal FXR is involved in the occurrence of AAD. | Communications Biology

Fig. 1: The decreased levels of ursodeoxycholic acid in both AAD patients and mouse serum suggest that intestinal FXR is involved in the occurrence of AAD.

From: Ursodeoxycholic acid alleviates aortic aneurysm and dissection through the intestinal farnesoid X receptor/ceramide synthase 2 axis

Fig. 1

A Validation process of this study flowchart. B Serum expression levels of ursodeoxycholic acid. (n = 7, per group). C Mouse serum expression levels of bile acid. (n = 10, per group). D Serum FGF19, MMP2, MMP9 levels in normal person, AA patients and AD patients (n = 30 per group). E–G ELISA results of FGF15, MMP2, and MMP9 during the 4-week BAPN-induced AAD process. (n = 10. per group). H Hepatic FXR and SHP mRNA expression in the AAD model mice induced by BAPN. (n = 6, per group). I Intestinal FXR, FGF15 and SHP mRNA expression in the AAD model mice induced by BAPN. (n = 6, per group). J Co-immunoprecipitation results from the intestine of AAD mice. Date in (E–H) and I are shown as the mean ± SEM. Statistical analysis was performed using two-tailed unpaired Student’s t test. Data in B and C 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).

Back to article page