Study on Sulforaphane Suppresses NLRP3 Inflammasome Activation in Gastric Mucosa Epithelial Cells Triggered by Helicobacter Pylori

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.