Curculigoside attenuates Helicobacter pylori-induced inflammation and apoptosis of gastric mucosal epithelial cells via NF-κB pathway

Abstract

Purpose: To investigate the possible effects and mechanisms of action of curculigoside (Cur) on gastric ulcers. Methods: Human gastric mucosal epithelial GES-1 cells were infected with Helicobacter pylori and then treated with Cur. Cell counting kit 8 (CCK-8), flow cytometry, and immunofluorescence assays were used to investigate the effect of Cur on cell viability and apoptosis after exposure to H. pylori. Inflammation status and reactive oxygen species (ROS) were assessed using enzyme-linked immunoassay (ELISA) and dichlorodihydrofluorescein (DCF) staining, respectively, while immunoblot and immunofluorescence assays were performed to determine the effect of Cur on the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway. Results: Cur significantly increased H. pylori-induced cell viability and inhibited H. pylori-induced inflammatory cytokine production (p < 0.01). Furthermore, Cur significantly suppressed H. pylori-induced ROS production and apoptosis (p < 0.01). Through the NF-κB pathway, Cur attenuated H. pylori-induced inflammation and apoptosis of gastric mucosal epithelial cells. Conclusion: In H. pylori infection, Cur treatment increases cell viability, reduces inflammatory cytokine production, suppresses ROS production, and inhibits apoptosis via NF-κB pathway. Further investigation using whole animal experiments would be needed to establish the role of Cur in the management of H. pylori-induced gastric ulcers.