Abstract: AIM: To study the effects of resveratrol (RES) on the mitochondrial damage, oxidative stress injury and NLRP3 inflammasome activation in colonic epithelial cells (Caco-2) induced by Escherichia coli O104∶H4.  METHODS: Caco-2 cells pre-treated with 200 μmol/L RES for 12 h, then cells were infected with 107 CFU/mL Escherichia coli O104∶H4 (MOI 10∶1) for 4 h. CCK-8 was used to detect the cell viability. qRT-PCR was performed to measure the expression levels of PGC1α, COX-4, NRF1, TFAM, SOD1 and HO-1 mRNA. Western blot was used to determine the expressions of NLRP3, CASP1 p20, CASP1 p10, pro-IL-1β and IL-1β. In addition, the mitochondrial membrane potential, oxygen consumption and ROS level were detected. RESULTS: Escherichia coli O104∶H4 infection could induce the expression levels of NLRP3, CASP1 p20, CASP1 p10, IL-1β protein and PGC1α, COX-4, NRF1 mRNA, and promote the oxygen consumption and ROS level, whereas significantly inhibit the cell viability, TFAM mRNA expression and the mitochondrial membrane potential (P<0.05). Furthermore, the expression levels of NLRP3, CASP1 p20, CASP1 p10, IL-1β protein and PGC1α, COX-4, NRF1 mRNA, and the oxygen consumption and ROS level were greatly decreased after treatment with RES in Caco-2 cells infected with Escherichia coli O104∶H4, whereas significantly induce the cell viability, TFAM mRNA expression and the mitochondrial membrane potential (P<0.05). In addition, ROS inhibitor (NAC) also could suppress the expressions of NLRP3 inflammasome and IL-1β. CONCLUSION: Escherichia coli O104∶H4 infection induces mitochondrial ROS release and NLRP3 inflammasome activation in Caco-2 cells, while RES exerts a preventive role in cells upon Escherichia coli O104∶H4 infection partially due to prevention of ROS production and activation of NLRP3 inflammasome.

Key words: resveratrol, Escherichia coli O104∶H4, colonic epithelial cells, NLRP3 inflammasome