An abalone viscera-derived sulfated Galactan alleviates Helicobacter pylori-induced gastric injury.

H. pylori infection is a major risk factor for chronic gastritis and gastric cancer, and antibiotic resistance severely limits the efficacy of current eradication therapies. In our present study, a sulfated galactan (named as AP-3) was isolated from abalone viscera with a novel structure. The results showed that the molecular weight (Mw) of AP-3 was approximately 10.2 kDa, which was composed of galactose (85.52%), glucose (6.65%), glucuronic acid (5.90%) and fucose (1.93%). The glycosidic linkage of the AP-3 main chain was →4)-α-D-galactose-(1 → with branches at C-3 of the backbone and sulfate groups at C-3 and C-6 of galactose. AP-3 significantly inhibited H. pylori adhesion to GES-1 cells, alleviated oxidative stress and mitochondrial damage, and reduced inflammatory responses. Animal experiments further showed that AP-3 attenuated gastric mucosal inflammation and oxidative injury and modulated H. pylori-associated alterations in gut microbiota composition. Transcriptomic analysis revealed enrichment of the NOD-like receptor signaling pathway following H. pylori infection, together with changes in inflammation-related gene expression after AP-3 treatment. Western blot analysis provided preliminary protein-level evidence of alterations in NOD1-NF-κB-associated inflammatory signaling after AP-3 treatment. In summary, AP-3 alleviated H. pylori-associated gastric injury and was accompanied by anti-adhesive, antioxidant, and anti-inflammatory effects, with preliminary findings suggesting changes in NOD1-NF-κB-associated inflammatory signaling.