Dietary succinoglycan riclin ameliorates spontaneous gut inflammation by restoring immune homeostasis in Period2-deficient mice

Dietary polysaccharides are promising candidates for managing inflammatory bowel disease (IBD). However, their efficacy is typically assessed in acute, chemically-induced models that poorly reflect human disease. We therefore evaluated the succinoglycan riclin in a novel spontaneous IBD model, Period2 -deficient ( Per2 −/− ) mice. Following a 4-month dietary intervention, riclin significantly ameliorated spontaneous intestinal inflammation. Treatment reduced inflammatory immune cell infiltration, suppressed oxidative stress, and enhanced antioxidant capacity. Riclin also restored intestinal barrier integrity by upregulating tight junction proteins and rescued the gut microbiota dysbiosis induced by Period2 deficiency. These findings demonstrate that riclin's benefits are associated with a multi-targeted mechanism that includes remodeling of the gut microbiome, reinforcement of the antioxidant system, and restoration of immune and barrier homeostasis. This study positions the dietary succinoglycan riclin as a potent prebiotic and functional food ingredient for microbiota-directed therapy of chronic gut inflammation.