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

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