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Abstract Title:

Allicin alleviated acrylamide-induced NLRP3 inflammasome activation via oxidative stress and endoplasmic reticulum stress in Kupffer cells and SD rats liver.

Abstract Source:

Food Chem Toxicol. 2021 Feb ;148:111937. Epub 2020 Dec 24. PMID: 33348049

Abstract Author(s):

Bo Nan, Chaoyue Yang, Lu Li, Haiqing Ye, Haiyang Yan, Minghua Wang, Yuan Yuan

Article Affiliation:

Bo Nan

Abstract:

Acrylamide (AA) in heat-processed food leads to widespread concerns due to its hepatotoxicity. Allicin, a plant-derived antioxidant, possesses a significant protective effect on AA-induced hepatotoxicity, but the mechanism is still unclear. Herein, we investigated the mechanism in Kupffer cells and SD rats liver. Molecular docking, molecular dynamics simulation and LigPlus software speculated that allicin inhibited the activity of CYP2E1 expression by binding to its amino acid residues Phe116, Phe207, Leu210, Phe298, Ala299, Thr303, Val364 and Phe478 through hydrophobic interactions. Allicin decreased the reactive oxygen species (ROS) release and CYP2E1 protein expression and then alleviated the appearance of OS. Meanwhile, allicin significantly reduced ERS characteristic proteins GRP78, CHOP and UPR branch IRE1α pathway key proteins p-IRE, p-ASK, TRAF2 and XBP-1s expression. Simultaneously, allicin ameliorated OS and ERS activation, which inhibited the activation of the MAPK and NF-κB pathways, and down-regulated JNK, ERK, p38, p65 and IκBα phosphorylation. Allicin pre-treatment inhibited AA-induced inflammation as evidenced by reducing NLRP3 inflammasome activation, decreasing Cleaved-Caspase-1 expression as well as IL-1β, IL-18, IL-6 and TNF-α secretion. Taken together, our data provide new insights into possible signaling pathways involved in allicin attenuating AA-induced hepatotoxicity invivo and in vitro.

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