Oxidative stress is closely associated with the initiation and progression of aging. Considerable interest centers in the potential application of natural polysaccharides in oxidative stress alleviation and senescence delay. Herein, LFP-05S, an acidic heteropolysaccharide from Lycii fructus, was purified and structurally characterized based on a combination strategy of molecular weight (MW) distribution, monosaccharide composition, methylation and NMR spectroscopy analysis. The dominant population of LFP-05S was composed of long homogalacturonan (HG) backbone interspersed with alternating sequences of intra-rhamnogalacturonans-I (RG-I) domains and branched arabinogalactan and arabinan. Orally supplied LFP-05S exhibited defensive modulation in paraquat (PQ)-damaged oxidative stress Caenorhabditis elegans by strengthening the internal defense systems. Under normal conditions, LFP-05S extended the lifespan without significant impairment of propagation. Overall, these results suggested LFP-05S and L. fructus are worth further exploration as promising redox-based candidates for the prevention and management of aging and related disorders.

Scavenging of oxidative stress by antioxidants may provide a therapeutic strategy for nonalcoholic fatty liver disease (NAFLD). Increasing evidence is supporting the potential application of natural resourced polysaccharides as promising prevention or treatment strategies against NAFLD. In the current study, an acidic heteropolysaccharide, LFP‐a1, was isolated and purified from Lycii fructus with successively hot water refluxing extraction, alcohol precipitation, protein removal, and DEAE‐52 cellulose chromatographic separation. LFP‐a1 was a complicated structured polysaccharide with an average MW of 4.74 × 104 Da and composed of 6 monosaccharides and 1 uronic acid. Preexposure of LFP‐a1 could increase the cell viability and reverse the abnormal oxidative stress though inhibition of mitochondrial‐mediated apoptotic pathway and correction of cell cycle progression against H₂O₂ hepatoxicity in NAFLD model L02 cells. Consistently, in vivo study in thioacetamide‐ (TAA‐) induced NAFLD model zebrafish larvae showed LFP‐a1 preserved the liver integrity and alleviated TAA‐induced oxidative stress through downregulation of abnormal apoptosis. These observations indicated the hepatoprotective activity of LFP‐a1, which may be applied for the prevention or treatment of NAFLD or other oxidative stress‐related diseases.