|Title:||Allicin Modifies the Composition and Function of the Gut Microbiota in Alcoholic Hepatic Steatosis Mice||Authors:||Panyod S.
|Issue Date:||2020||Publisher:||NLM (Medline)||Journal Volume:||68||Journal Issue:||10||Start page/Pages:||3088-3098||Source:||Journal of Agricultural and Food Chemistry||Abstract:||
The intestinal microbiome plays an important role in the pathogenesis of liver diseases. Alcohol intake induces gut microbiota dysbiosis and alters its function. This study investigated the antibiotic effect of allicin in mice with hepatic steatosis. Male C57BL/6 mice were administered an ethanol diet supplemented with allicin (5 and 20 mg/(kg bw day)) for 4 weeks. Allicin modified the gut microbiota composition. Cecal microbiota exhibited a positive correlation with alcohol and hepatic triacylglycerol, but were suppressed with allicin. Ethanol diet with 5 mg of allicin induced a lower intestinal permeability compared to the ethanol diet alone. Allicin mediated the lipopolysaccharide (LPS)-CD14-toll-like receptor 4 (TLR4)-induced hepatic inflammation pathway by reducing LPS, CD14, TLR4, and pro-inflammatory cytokines - tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6. However, hepatic inflammation primarily resulted from alcohol toxicity rather than LPS production in the gut. The prediction of functional profiles from metagenomic 16S ribosomal RNA (rRNA) data revealed different functional profiles in each group. The predicted aldehyde dehydrogenase tended to increase in alcoholic mice administered allicin. The predicted LPS-related pathway and LPS biosynthesis protein results exhibited a similar trend as plasma LPS levels. Thus, alcohol and allicin intake shapes the gut microbiota and its functional profile and improves the CD14-TLR4 pathway to alleviate inflammation in the liver. ? 2020 American Chemical Society.
|ISSN:||1520-5118||DOI:||10.1021/acs.jafc.9b07555||metadata.dc.subject.other:||Biochemistry; Cell death; Ethanol; Pathology; RNA; Aldehyde dehydrogenase; allicin; Gut microbiota; Hepatic steatosis; Hepatic triacylglycerol; Intestinal permeabilities; Pro-inflammatory cytokines; Tumor necrosis factors; Mammals; alcohol; allicin; interleukin 1beta; interleukin 6; sulfinic acid derivative; Tlr4 protein, mouse; toll like receptor 4; tumor necrosis factor; alcoholic fatty liver; animal; C57BL mouse; drug effect; genetics; human; immunology; intestine flora; liver; male; microbiology; mouse; Animals; Ethanol; Fatty Liver, Alcoholic; Gastrointestinal Microbiome; Humans; Interleukin-1beta; Interleukin-6; Liver; Male; Mice; Mice, Inbred C57BL; Sulfinic Acids; Toll-Like Receptor 4; Tumor Necrosis Factor-alpha
|Appears in Collections:||食品安全與健康研究所|
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