Metabolite acetyl- L-carnitine participates in Bifidobacterium animalis F1-7 to ameliorate atherosclerotic inflammation by downregulating theTLR4/NF-κB pathway

This study aimed to explore the effect of Bif. Animalis F1-7 on the improvement of atherosclerotic inflammation. Arteriosclerosis model ApoE^-/- mice were orally administered with Bif. Animalis F1-7 for 12 weeks. The probiotic intervention reduced the plaque areas in aorta and the accumulation of macrophages, and downregulated the expression of toll-like receptor 4 (TLR4)/nuclear factor‑κB (NFκB) pathway to reduce the levels of inflammatory factors. The widely-targeted metabolomics analysis showed that acetyl-L-carnitine (ALC) in the intestine of atherosclerotic mice was significantly increased after Bif. Animalis F1-7 intervention.Correlation analysis proved that ALC was associated with atherosclerotic inflammatory response. By using ox-LDL induced macrophage foam cells, we further verified that ALC could reduce lipid accumulation and inflammatory response in foam cells by downregulating the TLR4/NFκB pathway. Finally, our results revealed that Bif. Animalis F1-7 upregulated the metabolite ALC to downregulate the inflammatory responses, leading to the reduction of plaque accumulation of atherosclerosis.