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

• 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: acrylamide; kupffer cells (kcs); ros; nlrp3 inflammasome; the mapk pathway
• Online Access: http://dx.doi.org/10.1080/09540105.2019.1696284

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.