Sweet tea polysaccharides alleviate inflammation and regulate intestinal homeostasis via the gut-liver axis in ulcerative colitis mice

Abstract

Sweet tea ( Rubus suavissimus S. Lee) is a natural plant characterized by its low caloric content, high sweetness, and health-promoting properties, with polysaccharides being its primary active components. The sweet tea polysaccharides (STP), identified as an acidic heteropolysaccharide, demonstrated excellent anti-inflammatory potential in vitro by reducing NO, TNF-α, and IL-6 secretion and increasing IL-10 secretion in LPS-stimulated RAW264.7 cells. This study aimed to investigate the protective effects of STP and its underlying mechanism in mice with ulcerative colitis (UC). The results showed that STP ameliorated clinical symptoms in UC mice, including weight loss, disease activity index (DAI) scores, and pathological damage. Furthermore, STP bidirectionally modulated the secretion of key inflammatory factors (TNF-α, IL-6, IL-10) in both the colon and liver through the gut-liver axis. Additionally, STP enhanced the expression of tight junction proteins (ZO-1, Claudin-3, and Occludin) in the colonic epithelium, thereby repairing the impaired intestinal barrier and reducing endotoxin translocation. 16S rRNA sequencing analysis revealed that STP intervention enhanced gut microbiota diversity, increased the abundance of beneficial bacteria, and suppressed the growth of pathogenic bacteria. This microbial restructuring led to an increased production of short-chain fatty acids (SCFAs), which further contributed to the maintenance of intestinal microenvironment homeostasis and immune regulation. Our findings elucidate the synergistic role of STP in exerting anti-inflammatory effects and regulating gut microecology via the gut–liver axis, providing novel insights into natural product-based intervention strategies for UC and highlighting its promising application prospects as a functional food or therapeutic agent.