Acrylamide induces NLRP3 inflammasome activation via oxidative stress- and endoplasmic reticulum stress-mediated MAPK pathway in HepG2 cells

Acrylamide (AA) is one of the important products of the Maillard reaction. AA hepatotoxicity is related to inflammation, which can be indicated by the activation of NLRP3 inflammasome. In this study, AA activated NLRP3 inflammasome and released a large number of inflammatory factors in HepG2 cells. AA induced oxidative stress (OS) and endoplasmic reticulum stress (ERS) responses in HepG2 cells, accompanied by the activation of the MAPK signaling pathway. When HepG2 cells were pretreated with ROS (NAC) and ERS (4-PBA) inhibitors separately, the activation of NLRP3 inflammasome was inhibited. The MAPK signaling pathway was inhibited when OS and ERS were blocked. HepG2 cells pretreated with MAPK selective inhibitors led to the inhibition on the activation of NLRP3 inflammasome. Overall, we consider that AA induces the activation of NLRP3 inflammasome through the OS- and ERS-mediated MAPK signaling pathway in HepG2 cells. The hypothetical mechanism by which AA induced NLRP3 inflammasome activation in HepG2 cells. [Display omitted] •The NLRP3 inflammasome was activated by Acrylamide in HepG2 cells.•The activation of NLRP3 inflammasome induced by Acrylamide via OS- and ERS- mediated MAPK pathway.•Acrylamide evoked an increase in the level of proinflammatory cytokines.