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

Published on Feb 1, 2021in Food and Chemical Toxicology4.679
· DOI :10.1016/J.FCT.2020.111937
Bo Nan2
Estimated H-index: 2
(JLU: Jilin University),
Chaoyue Yang (JLU: Jilin University)+ 4 AuthorsYuan Yuan10
Estimated H-index: 10
(JLU: Jilin University)
Source
Abstract
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 in vivo and in vitro.
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