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

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...

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Veröffentlicht in:Journal of agricultural and food chemistry 2021-11, Vol.69 (43), p.12837-12852
Hauptverfasser: Yuan, Yuan, Lu, Li, Bo, Nan, Chaoyue, Yang, Haiyang, Yan
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Sprache:eng
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Zusammenfassung: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-κB 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-κB signaling pathway. In conclusion, allicin is highly effective in the treatment and prevention of AA-induced intestinal injury.
ISSN:0021-8561
1520-5118
DOI:10.1021/acs.jafc.1c05014