Phillyrin (PHY), also known as forsythin, is an active constituent isolated from the fruit of Forsythia suspensa (Thunb.) Vahl (Oleaceae). It exhibits anti-inflammatory, anti-viral, and antioxidant properties. However, the precise impact of PHY on colitis induced by dextran sodium sulfate (DSS) and its mechanism remain elusive. The present investigation revealed that PHY (12.5, 25.0, and 50.0 mg/kg) exhibited significant therapeutic efficacy in protecting mice against DSS-induced colitis. This effect was manifested as reduced weight loss, a shortened colon, increased secretion of inflammatory factors, increased intestinal permeability, and an enhanced disease activity index in mice with ulcerative colitis (UC). Molecular investigations have determined that PHY mitigates the nuclear translocation of nuclear factor kappa B, thereby downregulating myosin light-chain kinase-driven myosin light-chain phosphorylation. This mechanism results in the preservation of the integrity of the intestinal barrier. The outcomes of 16S rRNA sequencing suggest that PHY (50 mg/kg) augmented the relative abundance of certain probiotic strains, including Lactobacillaceae and Lachnospiraceae . Additionally, PHY supplementation elevated the short-chain fatty acid contents within the intestinal contents of mice with UC. In conclusion, pre-treatment with PHY may ameliorate the DSS-induced UC in mice by lowering the expression of inflammatory factors, protecting intestinal barrier function, and enhancing the structure of the intestinal flora. IMPORTANCE: The protective effect of phillyrin on DSS-induced colitis was explained for the first time, and the anti-inflammatory effect of phillyrin was demonstrated by fecal microbiota transplantation experiments mainly through intestinal flora.

Introduction: With inflammatory bowel disease (IBD) rising and current therapies limited, novel treatments are needed. Natural products are increasingly recognized as promising options for colitis. This study evaluated the therapeutic effects and mechanisms of lily polysaccharides (LP) in dextran sulfate sodium (DSS)–induced ulcerative colitis (UC). Methods: LP was administered in a DSS-induced UC model. Gut microbiota composition was profiled by sequencing, and metabolites were assessed with a focus on N8-acetylspermidine (N8AS). In vitro assays examined LP’s impact on N8AS production and intestinal barrier repair. Exogenous N8AS supplementation was tested for anti-colitic effects. Activation of the cyclic GMP–AMP synthase–stimulator of interferon genes (cGAS–STING) pathway and pro-inflammatory cytokine production were evaluated. Results: LP significantly alleviated colitic symptoms and restored microbial homeostasis, enriching beneficial taxa such as Bacteroides. LP markedly increased N8AS levels; in vitro, LP enhanced N8AS production, and exogenous N8AS supplementation alleviated colitis. Mechanistically, both LP and N8AS inhibited cGAS–STING pathway activation, reduced pro-inflammatory cytokines, and promoted intestinal barrier repair in vitro. Discussion: LP exerts anti-colitic activity through the microbiota/N8AS/cGAS–STING axis, linking microbial regulation, metabolic modulation, and immune signaling suppression. These findings support LP as a promising natural therapeutic for UC and provide novel insights into the beneficial effects and preliminary mechanisms of N8AS.

Anastomotic leak remains a major complication after colorectal resection, but established clinical and technical risk factors do not fully explain why some repairs fail during early healing. This review treats perioperative microbiota as part of a local host-microbe wound environment at the colorectal anastomosis rather than as a broad gut microbiome signal. Literature was identified through PubMed and Web of Science searches covering 1 January 2010–6 July 2026, using terms combining colorectal anastomosis, anastomotic leak, microbiota, microbiome, and host-microbe interactions. Evidence was tiered by directness to the anastomotic wound, distinguishing stool-based proxy signals from mucosal, tissue-adjacent, and functional measurements. Stool and broader luminal profiles provide indirect signals for suture-line events unless paired with site-aware sampling. Mucosal, mucus, and tissue-adjacent studies move closer to the repair site but remain mostly exploratory and associative. Animal and in vitro work supports plausible mechanisms, including collagenase activity, biofilm-like persistence, metabolite signaling, inflammatory modulation, and extracellular matrix injury, but does not establish human clinical causality. Current evidence justifies better perioperative sampling, function-aware microbial analysis, and integration with conventional leak-risk factors; it does not justify routine microbiome-guided risk stratification or leak-prevention interventions. The most useful next step is longitudinal, site-aware human work anchored to standardized leak outcomes and surgical context.