潰瘍性大腸炎

Ulcerative colitis (UC) is a chronic inflammatory bowel disease whose complex etiology is increasingly linked to gut microbiota dysbiosis. While conventional pharmacological treatments often face limitations due to side effects, cost, and variable efficacy, synbiotics combinations of probiotics and prebiotics have emerged as a promising therapeutic strategy to restore intestinal homeostasis. This review synthesizes evidence from recent animal model studies to elucidate the multifaceted mechanisms and superior efficacy of synbiotic interventions in ameliorating colitis. We demonstrate that synbiotics, whether composed of traditional components like lactobacilli, bifidobacteria, inulin, and fructooligosaccharides, or novel formulations involving exopolysaccharides, engineered glucans, and specific fatty acid-producing consortia, consistently outperform their individual components. The therapeutic effects are mediated through a synergistic restoration of gut microbial diversity, enhanced production of protective metabolites (especially short-chain fatty acids and secondary bile acids), fortification of the intestinal barrier via upregulation of tight junction proteins, and modulation of key immune pathways, including NF-κB, MAPK, and AhR. Furthermore, we highlight the advanced strategy of microencapsulation using prebiotic wall materials to enhance probiotic viability and targeted colonic delivery. The collective evidence positions synbiotics not merely as nutritional supplements but as sophisticated, multi-targeted therapeutics. This review underscores the critical need for future research to focus on structure-function relationships, precision synbiotic formulations tailored to individual microbiota profiles, and robust human clinical trials to translate these compelling preclinical results into effective clinical management strategies for UC.

Inflammatory bowel disease (IBD), particularly ulcerative colitis (UC), remains a major global health challenge characterized by chronic, relapsing inflammation of the colonic mucosa. Although conventional pharmacotherapies, including corticosteroids and mesalamine are widely used for disease management, their long-term efficacy is often limited by systemic adverse effects, treatment resistance and reduced patient responsiveness. Consequently, growing attention has been directed toward plant-derived bioactive compounds owing to their multi-target therapeutic potential and distinct structural mechanisms. This review highlights the pharmacological potential of Gossypium barbadense L. (Egyptian cotton) root extract as a potential phytotherapeutic candidate for the management of colitis. We summarize current evidence regarding the molecular mechanisms through which its major phytochemical constituents, particularly gossypol and related polyphenolic compounds that modulate inflammatory and oxidative stress pathways. The principal mechanisms include inhibition of NF-κB and COX-2 signaling, enhancement of endogenous antioxidant defense system, preservation of intestinal epithelial barrier integrity and restoration of immune homeostasis. In addition, the immunomodulatory and redox-regulating properties of G. barbadense phytoconstituents are discussed in the context of intestinal inflammation. Furthermore, this review integrates recent advances in network pharmacology to elucidate the multi-component, multi-target interactions underlying the therapeutic effects of G. barbadense. By consolidating current preclinical evidence and computational pharmacology approaches, this review highlights the potential of G. barbadense root as a prospective source of novel therapeutic agent for IBD while identifying key knowledge gaps that should be addressed before clinical translation.

In patients with acute severe ulcerative colitis (ASUC) who have received infliximab rescue therapy, the need for and timing of further steroid therapy is unclear. This brief communication explores contemporary clinical practice across Australia regarding corticosteroid management following rescue therapy in ASUC. By describing variability in real-world practice patterns and potential risks and benefits of different approaches, this article highlights current evidence gaps and the need for further studies to better inform clinical practice.

ObjectiveThis prospective study evaluated the therapeutic efficacy of Diosgenin in mitigating Oxazolone-induced ulcerative colitis in male BALB/c mice.MethodMice aged 10-11 weeks were randomized into five groups and subjected to a nine-day protocol involving skin sensitization and intra-rectal Oxazolone challenge. Diosgenin was administered orally at 3 mg/kg and 30 mg/kg twice daily, with Tofacitinib at 60 mg/kg as a reference control. Disease severity was assessed via clinical activity scores, which include tested parameters.ResultsOxazolone-induced acute colitis was characterized by significant weight loss, increased diarrhoea scores, and an >8-fold increase in rectal bleeding scores compared with vehicle-treated mice, confirming successful disease induction (p < 0.05). Diosgenin-treated mice showed significant recovery. Disease Activity Index (DAI) scores improved by 40% in the 3 mg/kg Diosgenin group, 45% in the 30 mg/kg Diosgenin group, and 67% in the Tofacitinib-treated group by Day 2. Stool consistency improved by 52%, 33%, and 49% on Day 1, and by 33%, 61%, and 64% on Day 2 in the 3 mg/kg and 30 mg/kg Diosgenin groups, and the 60 mg/kg Tofacitinib groups respectively. Molecular analysis revealed a dose-dependent suppression of Th2 cytokines: IL-4 levels were reduced by 71%, 90%, and 86%, and IL-13 levels by 75%, 79%, and 90% in the Diosgenin 3mg/kg and 30 mg/kg groups, and Tofacitinib 60 mg/kg group respectively. Diosgenin markedly suppressed colonic pSTAT3 expression, with reductions of 92% and 99%, in the Diosgenin 3mg/kg and 30 mg/kg groups and >90% in the Tofacitinib 60 mg/kg group.ConclusionThese findings suggest Diosgenin offers substantial protection against Oxazolone-induced colitis via cytokine modulation and pSTAT3 inhibition, highlighting its potential as a natural anti-inflammatory agent for colitis management.

Ulcerative colitis (UC) is an immune-mediated chronic inflammatory bowel disease that severely impairs patients' quality of life. Efficient oral colon-targeted delivery systems are urgently needed to improve local therapeutic efficacy while minimizing systemic exposure. Herein, we developed a pH-responsive Eudragit S100-coated coacervate microdroplet system for the oral delivery of natural Bletilla striata polysaccharide (BSP), termed BSP@EU-Coac. The optimized BSP@EU-Coac microdroplets exhibited a spherical morphology with an average hydrodynamic diameter of 3.86 ± 0.82 μm, an encapsulation efficiency of 85.03 ± 3.66%, and a drug loading capacity of 9.29 ± 0.93%. In vitro release studies showed that BSP@EU-Coac effectively limited premature BSP release under simulated gastric and small intestinal conditions, while achieving pH-triggered sustained release in simulated colonic medium, with a cumulative release of approximately 88.25% within 96 h. In vitro assays further demonstrated that BSP@EU-Coac showed good cytocompatibility at the working concentration and markedly reduced intracellular ROS levels, with ROS fluorescence intensity decreased by 53.95% and 51.13% in RAW264.7 macrophages and Caco-2 cells, respectively. After oral administration, fluorescence imaging confirmed that BSP@EU-Coac preferentially accumulated in the inflamed colon and maintained detectable colonic retention for up to 24 h. In a DSS-induced colitis mouse model, BSP@EU-Coac significantly alleviated UC symptoms, as evidenced by improved body weight recovery, reduced disease activity index, and restoration of colon length from 4.99 ± 1.23 cm in the model group to 8.66 ± 1.92 cm. Mechanistically, BSP@EU-Coac modulated macrophage polarization by reducing the M1-like CD86⁺CD206⁻ population from 29.26% to 8.95% and increasing the M2-like CD86⁻CD206⁺ population to 20.70%, accompanied by suppressed pro-inflammatory cytokine expression, enhanced tight junction protein expression, reduced oxidative stress, and partial restoration of gut microbiota homeostasis. Overall, this study demonstrates that BSP@EU-Coac is a promising oral colon-targeted polysaccharide delivery platform for UC therapy through integrated regulation of oxidative stress, immune response, epithelial barrier repair, and gut microbiota.