Scorias spongiosa, a type of edible fungus, is beneficial for intestinal health. However, the mechanisms by which polysaccharides derived from S. spongiosa contribute to the integrity of the intestinal barrier have been little investigated. In the present study, 40 C57BL/6J mice were assigned into five groups: (1) Normal; (2) Dextran sulfate sodium (DSS)Administration; (3) DSS + Uncapped polysaccharides; (4) DSS + Low microcapsules; (5) DSS + High microcapsules. After one week of administration of S. spongiosa polysaccharides, all mice, excluding the Normal group, had free access to the drinking water of 3.5% DSS for seven days. Serum and feces were then taken for analysis. Scanning electron microscopy analysis indicated the structure of the micro-capped polysaccharides with curcumin was completed with a rough surface, which differs from the uncapped polysaccharides. Noticeably, S. spongiosa polysaccharides enhanced intestinal barrier integrity as evidenced by increasing the protein levels of Claudin-1, ZO-1 and ZO-2. Low-capped polysaccharides mitigated the DSS-induced oxidative stress by increasing catalase (CAT) concentration and decreasing malondialdehyde (MDA) and myeloperoxidase (MPO) concentrations. Besides, DSS treatment caused a disturbance of inflammation and the contents of IL-1β, IL-6, TNF-α and CRP were downregulated and the contents of IL-4, IL-10 and IFN-γ were upregulated by S. spongiosa polysaccharides. Research on the potential mechanisms indicated that S. spongiosa polysaccharides inhibited the DSS-triggered activation of NF-κB signaling. Moreover, the JAK/STAT1 and MAPK pathways were suppressed by S. spongiosa polysaccharides in DSS-challenged mice, with Lcap showing the strongest efficacy. 16S rDNA amplicon sequencing revealed that the richness and diversity of the microbial community were reshaped by S. spongiosa polysaccharide ingestion. Therefore, our study substantiated that S. spongiosa polysaccharides exhibited protective effects against colitis mice by reshaping the intestinal microbiome and maintaining the balance of intestinal barrier integrity, antioxidant capacity and colonic inflammation through regulation of the NF-κB–STAT1–MAPK axis.

This study was designed to characterize the hepatoprotective effects of alkali-soluble polysaccharides from submerged mycelium of edible mushroom Lepista sordida (LMADa1) against CCl4-induced oxidative damage in mice. Structural characterization revealed that LMADa1 had an average molecular weight (Mw) of 1442 kDa and consisted of glucose (57.9%), xylose (31.8%), and small amounts of rhamnose, arabinose, galactose, glucuronic acid, and galacturonic acid (1.2–3.1%). The FT-IR and 2D NMR confirmed that LMADa1 was composed of Xylp, Araf, 4-O-Me-α-D-GlcpA, (1→4)-linked β-D-Glcp, and (1→4)-α-D-GalA, and β-glycosidic linkages between these sugar units. The LMADa1 had notable effects against 1,1-dephenyl-2-picryhydrazyl (DPPH) radical scavenging, hydrogen peroxide scavenging, lipid peroxidation inhibitory ability, reducing power and Fe2+ chelating activity. These effects were further verified by suppressing CCl4-induced oxidative liver damage in mice at 100 and 200 mg/kg. Administration of LMADa1 in mice prior to CCl4 significantly prevented the CCl4-induced elevation in serum alanine aminotransferase, aspartate aminotransferase, and hepatic malondialdehyde. Mice treated with LMADa1 demonstrated increased activities in superoxide dismutase and glutathione peroxidase in the liver. This also prevented CCl4-induced oxidative liver histological alteration. The results suggest that LMADa1 protects the liver from CCl4-induced damage via antioxidant mechanisms.