Bifidobacterium
animalis subsp. lactis F1–7 Alleviates
Lipid Accumulation in Atherosclerotic
Mice via Modulating Bile Acid Metabolites to Downregulate Intestinal
FXR
The dysfunction of intestinal microbiota and bile acid
metabolism
is related to the pathogenesis of atherosclerosis. This study we explored
the mechanism of Bifidobacterium animalis subsp. lactis F1–7 (Bif. animalis F1–7),
improving atherosclerosis by regulating the bile acid metabolism and
intestinal microbiota in the ApoE–/– mice.
The Bif. animalis F1–7 effectively reduced
aortic plaque accumulation and improved the serum and liver lipid
levels in atherosclerotic mice. The untargeted metabolomics revealed
that Bif. animalis F1–7 reduced the glycine-conjugated
bile acids and the levels of differential metabolite lithocholic acid
(LCA) significantly. Downregulation of LCA decreased the intestinal
levels of the farnesoid X-activated receptor (FXR) and regulated the
bile acid metabolism through the FXR/FGF15/CYP7A1 pathway. Furthermore,
the 16srRNA gene sequencing analysis revealed that structural changes
in intestinal microbiota with an increase in the abundance of Bifidobacterium, Lactobacillus, Faecalibaculum, Desulfovibrio, and a decrease
in Dubosiella, Clostridium_sensu_stricto_1, and Turicibacter following the Bif. animalis F1–7 intervention. Correlation analysis showed that the changes
in intestinal microbiota mentioned above were significantly correlated
with bile acid metabolism in atherosclerotic mice. In conclusion,
this study sheds light on the mechanisms by which Bif. animalis F1–7 regulates atherosclerosis.