Abstract: OBJECTIVE To study the effects of sulforaphane(SFP) on the mitochondrial damage, oxidative stress injury and NLRP3 inflammasome activation in gastric mucosa epithelial cells(GES-1) induced by Helicobacter pylori infection. METHODS GES-1 cells pre-treated with 100 ng·mL^-1 of SFP for 12 h, then cells were infected with 10⁹ CFU·mL^-1 of Helicobacter pylori for 6 h. CCK8 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 blotting 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 Helicobacter pylori infection could evidently 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, SOD1, HO-1, TFAM mRNA expression and the mitochondrial membrane potential(P<0.05). Furthermore, the expression levels of NLRP3, IL-1β protein and PGC1α, COX-4, NRF1 mRNA, and the oxygen consumption and ROS level were greatly decreased after treatment with SFP in GES-1 cells induced with Helicobacter pylori infection, whereas significantly induced the cell viability, SOD1, HO-1, 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 SFP can improve the inflammatory response of GES-1 cells triggered by Helicobacter pylori infection by reducing mitochondrial damage and ROS levels.