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Figure 4. Histopathological analysis of L. johnsonii on liver tissue in hypercholesterolemic mice. H&E staining of the liver, 200×. H&E:
Hematoxylin-eosin.
Figure 5. The effect of L. johnsonii CCFM1376 on the bile acid composition in the enterohepatic circulation of hypercholesterolemic mice.
(A) Unconjugated bile acid composition in the liver; (B) Total bile acid in the liver; (C) bile acid proportion in the liver; (D) unconjugated
bile acid composition in the serum; (E) Total bile acid in the serum; (F) bile acid proportion in the serum; (G) unconjugated bile acid
composition in the ileum; (H) Total bile acid in the ileum; (I) bile acid proportion in the ileum; (J) unconjugated bile acid composition in
the feces; (K) Total bile acid in the feces; (L) bile acid proportion in the feces. Groups with the same lowercase letter did not exhibit
significant differences, whereas those with different letters indicated significant differences (P < 0.05).
L. johnsonii CCFM 1376 alters the expression profile of genes involved in the regulation of bile acid
synthesis mediated by the FXR pathway
Small heterodimer partner (SHP) and fibroblast growth factor 15 (FGF15) are key signaling molecules in the
liver FXR and intestinal FXR regulatory pathways, respectively. A study on the regulation of cholesterol
metabolism by the active component of Pu-erh tea, theabrownin, has shown that the intestinal FXR-FGF15
[19]
and the liver FXR-SHP can dually regulate the expression of CYP7A1 . To investigate the impact of L.
johnsonii CCFM1376 on the hepatic and intestinal FXR signalling mechanism in mice, the relative
expression levels of the FXR and SHP in the liver, FXR and FGF15 in the ileum, and the critical enzyme gene
CYP7A1 involved in liver bile acid production were measured. Compared to the model group, L. johnsonii
CCFM1376 significantly downregulated the relative expression levels of FXR and FGF15 in the mouse
ileum, but did not significantly affect the relative expression levels of hepatic FXR and its key regulatory

