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

作　　者：Xi Liang Zhe Zhang Xiaoying Tian Qingyu Cui Haiyan Lu Maozhen Zhao Tongjie Liu Huaxi Yi Pimin Gong Lanwei Zhang 

机构地区：[1]Department of Nutrition and Food Hygiene,School of public health,Qingdao University,Qingdao 266071,China [2]College of Food Science and Engineering,Ocean University of China,Qingdao 266003,China

出　　处：《Food Science and Human Wellness》2024年第2期813-822,共10页食品科学与人类健康（英文）

基　　金：supported by Shandong Taishan industry leading talent project(LJNY202101);the National Key R&D of China(2018YFC0311201)。

摘　　要：This study aimed to explore the effect of Bifidobacterium animalis F1-7 on the improvement of atherosclerotic inflammation.Arteriosclerosis model ApoE^(-/-)mice were orally administered with B.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 factorκB(NF-κB)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 B.animalis F1-7 intervention.Correlation analysis proved that ALC was associated with atherosclerotic inflammatory response.By using oxidized low density lipoprotein induced macrophage foam cells,we further verified that ALC could reduce lipid accumulation and inflammatory response in foam cells by downregulating the TLR4/NF-κB pathway.Finally,our results revealed that B.animalis F1-7 upregulated the metabolite ALC to downregulate the inflammatory responses,leading to the reduction of plaque accumulation of atherosclerosis.

关 键 词：Bifidobacterium animalis F1-7 Atherosclerosis INFLAMMATION METABONOMICS ACETYL-L-CARNITINE 

分 类 号：R54[医药卫生—心血管疾病] TS201.3[医药卫生—内科学]