摘要
Ulcerative colitis is one of the classical chronic inflammatory bowel diseases, has complex etiology involving immune dysfunction and gut microbiota dysbiosis.Traditional medicine polysaccharides have shown promising potential to alleviate intestinal inflammation associated with UC.However, there is still insufficient reporting on how the polysaccharides from Phyllanthus emblica can exert therapeutic and repairing effects by regulating gut microbiota.So, the current study was conducted to assess the therapeutic potential of Phyllanthus emblica fruit polysaccharide (PEP) on UC and its influence on the gut microbiota and metabolite profiles in a DSS-induced mice UC model.This study assessed the clinical, histopathological, inflammatory/oxidative stress indices, and analyzed gut microbiota by 16S rRNA sequencing and fecal metabolites by untargeted metabolomics in four mouse groups with oral PEP treatment in DSS-induced UC model.PEP treatment significantly alleviated clinical severity, evidenced by decreased level of disease activity index, restoring the length of colon, and improvement in histopathology.It strengthened intestinal barrier wholeness by upregulating tight junction proteins (ZO-1, Occludin) and suppressed colonic proinflammatory cytokines (TNF-α, IL-1β, IL-6), Myeloperoxidase and malondialdehyde.In addition, multi-omics analysis revealed that PEP alleviated UC by remodeling the gut microbiota and its metabolic function.PEP selectively enriched beneficial commensals such as Bacteroides acidifaciens and Paraprevotella clara, and increasing the SCFA-producing, rhamnose, histidine metabolism, and peptidoglycan.PEP selectively enriched beneficial commensals such as Bacteroides acidifaciens, and Paraprevotella clara.Then, that supported the ecological stability of the consortium, which subsequently increased the production of SCFA, rhamnose, histidine metabolism, and peptidoglycan, contributing to the alleviation of intestinal inflammation.In summary, PEP alleviates UC by first strengthening the intestinal colonization of core beneficial bacteria, which in turn produce metabolites that directly repair the epithelial barrier and resolve inflammation.