4.7 Article

Allicin Ameliorates Intestinal Barrier Damage via Microbiota-Regulated Short-Chain Fatty Acids-TLR4/MyD88/NF-κB Cascade Response in Acrylamide-Induced Rats

期刊

JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
卷 69, 期 43, 页码 12837-12852

出版社

AMER CHEMICAL SOC
DOI: 10.1021/acs.jafc.1c05014

关键词

acrylamide (AA); allicin; intestinal barrier; gut microbiota; short-chain fatty acids; TLR4/MyD88/NF-kappa B

资金

  1. National Natural Science Foundation of China [32172322, 31571939]

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The study demonstrates that allicin can alleviate AA-induced intestinal barrier breakage, regulate the microbiota-SCFAs signaling, decrease the expression of inflammatory cytokines, and reduce intestinal injury and inflammation.
Acrylamide (AA) is a heat-induced toxicant, which can cause severe damage to health. In the present study, SD rats were used to investigate the potential therapeutic effects of allicin dietary supplementation in the rats with AA-induced intestinal injury. The elevated expression of occludin, claudin-1, zonula occludens-1 (ZO-1), mucin 2, and mucin 3 indicated that oral allicin alleviated the intestinal epithelial barrier breakage induced by AA, compared with the AA-treated group. In the gut microbiota, Bacteroides, Escherichia_Shigella, Dubosiella, and Alloprevotella related to the synthesis of short-chain fatty acids (SCFAs) were negatively affected by AA, while allicin regulated cascade response of the microbiota-SCFAs signaling to reverse the reduction of acetic acid and propionic acid by AA treatment. Allicin also dramatically down-regulated the expression of Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), NF-kappa B signaling pathway proteins, and proinflammatory cytokines by promoting the production of SCFAs in AA-treated rats. Allicin relieved the intestinal barrier injury and inflammation caused by AA as evidenced by the regulation cascade response of the microbiota-SCFAs-TLR4/MyD88/NF-kappa B signaling pathway. In conclusion, allicin is highly effective in the treatment and prevention of AA-induced intestinal injury.

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