Acrylamide induced the activation of NLRP3 inflammasome via ROS-MAPKs pathways in Kupffer cells

Acrylamide (AA) is an important product of the Maillard reaction. Studies have demonstrated that AA caused oxidative stress damage in liver, which in turn triggered an inflammatory response, and the activation of NOD-like receptor protein-3 (NLRP3) inflammasome played a key factor in regulating infl...

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Main Authors: Nan Bo, Hong Yilin, Yan Haiyang, Yuan Yuan
Format: Article
Language:English
Published: Taylor & Francis Group 2020-01-01
Series:Food and Agricultural Immunology
Subjects:
Online Access:http://dx.doi.org/10.1080/09540105.2019.1696284
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author Nan Bo
Hong Yilin
Yan Haiyang
Yuan Yuan
author_facet Nan Bo
Hong Yilin
Yan Haiyang
Yuan Yuan
author_sort Nan Bo
collection DOAJ
description Acrylamide (AA) is an important product of the Maillard reaction. Studies have demonstrated that AA caused oxidative stress damage in liver, which in turn triggered an inflammatory response, and the activation of NOD-like receptor protein-3 (NLRP3) inflammasome played a key factor in regulating inflammation. Therefore, we hypothesized NLRP3 inflammasome activation was involved in AA-induced inflammatory response. AA induced the reactive oxygen species (ROS) overproduction, accompanied by the MAPK pathway activation, which resulted in NLRP3 inflammasome formation, and eventually increased IL-1β and IL-18 release. The activation of the MAPK pathway was inhibited when using ROS scavenger (NAC). And when MAPK selective inhibitors were used, KCs viability was increased though AA-treated. Meanwhile the NLRP3 inflammasome activation was inhibited, which decreased the release of the cellular inflammatory secretion factors IL-1β and IL-18. Overall, the activation of ROS-MAPK-NLRP3-IL-1β signalling axis induced by AA plays an important role in the process of inflammation. Signaling pathways involved in inflammation induced by AA. After AA stimulated KCs, a large amount of ROS were released. ROS activated MAPK signaling pathway to promote the activation of NLRP3 inflammasome. Activation of NLRP3 signaling activated Caspase-1, resulting in the maturation of IL-1β and IL-18. The activation of NLRP3 inflammasome was inhibited and the levels of cytoinflammatory factor IL-1β and IL-18 were decreased when using MAPK selective inhibitors.
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spelling doaj.art-3f8a2b52a4984718ae3edf3b8db7a7d72022-12-21T18:00:11ZengTaylor & Francis GroupFood and Agricultural Immunology0954-01051465-34432020-01-01311456210.1080/09540105.2019.16962841696284Acrylamide induced the activation of NLRP3 inflammasome via ROS-MAPKs pathways in Kupffer cellsNan Bo0Hong Yilin1Yan Haiyang2Yuan Yuan3College of Food Science and Engineering, Jilin UniversityCollege of Food Science and Engineering, Jilin UniversityCollege of Food Science and Engineering, Jilin UniversityCollege of Food Science and Engineering, Jilin UniversityAcrylamide (AA) is an important product of the Maillard reaction. Studies have demonstrated that AA caused oxidative stress damage in liver, which in turn triggered an inflammatory response, and the activation of NOD-like receptor protein-3 (NLRP3) inflammasome played a key factor in regulating inflammation. Therefore, we hypothesized NLRP3 inflammasome activation was involved in AA-induced inflammatory response. AA induced the reactive oxygen species (ROS) overproduction, accompanied by the MAPK pathway activation, which resulted in NLRP3 inflammasome formation, and eventually increased IL-1β and IL-18 release. The activation of the MAPK pathway was inhibited when using ROS scavenger (NAC). And when MAPK selective inhibitors were used, KCs viability was increased though AA-treated. Meanwhile the NLRP3 inflammasome activation was inhibited, which decreased the release of the cellular inflammatory secretion factors IL-1β and IL-18. Overall, the activation of ROS-MAPK-NLRP3-IL-1β signalling axis induced by AA plays an important role in the process of inflammation. Signaling pathways involved in inflammation induced by AA. After AA stimulated KCs, a large amount of ROS were released. ROS activated MAPK signaling pathway to promote the activation of NLRP3 inflammasome. Activation of NLRP3 signaling activated Caspase-1, resulting in the maturation of IL-1β and IL-18. The activation of NLRP3 inflammasome was inhibited and the levels of cytoinflammatory factor IL-1β and IL-18 were decreased when using MAPK selective inhibitors.http://dx.doi.org/10.1080/09540105.2019.1696284acrylamidekupffer cells (kcs)rosnlrp3 inflammasomethe mapk pathway
spellingShingle Nan Bo
Hong Yilin
Yan Haiyang
Yuan Yuan
Acrylamide induced the activation of NLRP3 inflammasome via ROS-MAPKs pathways in Kupffer cells
Food and Agricultural Immunology
acrylamide
kupffer cells (kcs)
ros
nlrp3 inflammasome
the mapk pathway
title Acrylamide induced the activation of NLRP3 inflammasome via ROS-MAPKs pathways in Kupffer cells
title_full Acrylamide induced the activation of NLRP3 inflammasome via ROS-MAPKs pathways in Kupffer cells
title_fullStr Acrylamide induced the activation of NLRP3 inflammasome via ROS-MAPKs pathways in Kupffer cells
title_full_unstemmed Acrylamide induced the activation of NLRP3 inflammasome via ROS-MAPKs pathways in Kupffer cells
title_short Acrylamide induced the activation of NLRP3 inflammasome via ROS-MAPKs pathways in Kupffer cells
title_sort acrylamide induced the activation of nlrp3 inflammasome via ros mapks pathways in kupffer cells
topic acrylamide
kupffer cells (kcs)
ros
nlrp3 inflammasome
the mapk pathway
url http://dx.doi.org/10.1080/09540105.2019.1696284
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