Polygonum bistorta L. ( P. bistorta ) has long been used as a medicinal herb with hemostatic, antidiarrheal, and anti-inflammatory properties. Improper antibiotic use can cause intestinal inflammation and disrupt the intestinal epithelial barrier, resulting in the progression of various intestinal diseases. To evaluate the effects of P. bistorta neutral polysaccharide (PBP) fraction in an antibiotic-induced Caco-2 cell barrier model and further explore its related mechanisms, PBP fraction was extracted with hot water and then precipitated with ethanol. The crude extract was subjected to successive purification procedures, including anion exchange and gel filtration chromatography. The preliminary physicochemical characterization was performed through a combination of structural analytical techniques. The pharmacological efficacy of PBP fraction was systematically evaluated via permeability assessment and tight junction (TJ) protein validation in an antibiotic-induced Caco-2 intestinal barrier model. Monosaccharide composition analysis revealed that the PBP fraction consisted primarily of glucose, arabinose, and galactose. Pharmacological investigations revealed that the candidate polysaccharide fraction at 400 μg/mL significantly attenuated antibiotic-induced cellular cytotoxicity and reversed the impaired transepithelial electrical resistance (TEER) caused by clindamycin, concurrently reducing the paracellular permeability of FITC-dextran. Mechanistically, PBP treatment markedly upregulated the expression of key TJ proteins, including ZO-1, Occludin, and Claudin-1, as confirmed by Western blot analysis. This study demonstrated that a polysaccharide fraction from P. bistorta ameliorated antibiotic-induced intestinal barrier dysregulation, highlighting its potential as a functional food ingredient for gut health. • We isolated and characterized a novel neutral polysaccharide fraction from P. bistorta . • PBP fraction attenuates antibiotic induced intestinal barrier damage in Caco-2 cells. • PBP fraction significantly upregulated tight junction proteins in intestinal barrier damage model.
Yang et al. (Fri,) studied this question.