Ulcerative colitis (UC) is an inflammatory bowel disease that is persistent and nonspecific. There are several medications available for the treatment of UC. However, conventional UC medications have substantial adverse effects, low clinical effectiveness, and a high recurrence rate. Therefore, it is critical to discover new medicines that are both safe and effective for UC patients. Natural polysaccharides offer a wide range of pharmacological benefits, including anti-inflammatory, anti-virus, anti-tumor, anti-aging, immune enhancement, and gut flora regulation. In the therapy of UC, natural polysaccharides can modulate inflammatory factors, the immune system, and intestinal flora, and preserve the intestinal mucosa. It demonstrates a good curative effect and is of safety to use, thereby being a potential treatment for UC patients. This paper covers the structure, the pharmacological effects on UC, and the mechanisms of natural polysaccharides. Finally, limitations, challenges, and perspectives are discussed. It is hoped that the findings of this publication will inspire more natural polysaccharides research and provide a theoretical foundation for the creation of new UC medications.
Objective The present study was performed to evaluate the effect of intestinal microbiota transplantation (IMT) on intestinal flora and inflammatory factor levels in patients with ulcerative colitis (UC). Methods In this study, 94 UC patients who attended the Department of Proctology or the Department of Gastroenterology departments of Sinopharm Dongfeng General Hospital between April 2021 and April 2022 were identified as research participants and were assigned to the control or Research Groups via the random number table method, with 47 cases in each group. Interventions included oral mesalamine for patients in the control group and oral mesalamine plus IMT for those in the research group. Outcome measures included clinical efficacy, intestinal microbiota score, enteroscopy score, Sutherland index, inflammatory factor level, intestinal mucosal barrier function level, and adverse reactions. Results Mesalamine plus IMT was associated with significantly higher treatment efficiency (97.8%) versus mesalamine alone (80.85%) (P<0.05). Mesalamine plus IMT provided a better intestinal microbiota balance and milder disease symptoms versus mesalamine, as evidenced by the significantly lower intestinal microbiota scores, colonoscopy scores, and Sutherland index (P<0.05). In post-treatment, patients with IMT exhibited more mitigated inflammatory responses than those without, as shown by the higher levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-17 (IL-17), and interleukin-23 (IL-23) (P<0.05). Significantly lower D-lactate and serum diamine oxidase (DAO) levels were observed after IMT intervention than those with mesalamine alone (P<0.05). IMT features no significant increase in adverse effects than the control group (P>0.05). Conclusion IMT efficiently ameliorates the intestinal microbiota conditions of UC patients, mitigates inflammatory responses in the body, and facilitates the restoration of intestinal mucosal barrier function with no significant increase in adverse effects.
IntroductionUlcerative colitis (UC) is an inflammatory bowel disease characterized by recurrent and remitting inflammation of the mucosa of the colon and rectum, the incidence of which is on the rise. Glucagon-like peptide-2 (GLP-2) is a newly discovered neurotrophic factor, but its efficacy and mechanism of action in UC remain unclear. In this study, we investigated the protective effects and potential targets of GLP-2 on dextran sodium sulfate (DSS)-induced UC in mice through integrative analysis.MethodsThe effects of GLP-2 on UC were assessed by calculating the disease activity index, colonic mucosal damage index, and pathological histological scores. Enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry were used to detect the expression of GLP-2, nuclear factor kappa-B (NF-κB), interleukin-6 (IL-6), and signal transducer and activator of transcription-3 (STAT3). The 16SrRNA gene was used to detect changes in gut microbiota in mouse colonic tissues, and oral glucose tolerance test (OGTT) blood glucose levels were used to analyze the differences in flora.ResultsThe results showed that GLP-2 could reduce the inflammation of UC mice, which may be achieved by inhibiting the potential targets of NF-κB, and Janus kinase (JAK)/STAT3 inflammatory pathways, regulating sugar metabolism, increasing dominant species, and improving microbial diversity.DiscussionThis study provides new insight into the potential of GLP-2 for achieving more ideal UC treatment goals in future.
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