Geniposide (GE) has potential efficacy in treating ulcerative colitis (UC). However, its reactivity can be affected by rapid degradation after oral administration. Furthermore, increasing oral doses may lead to hepatotoxicity. Thus, We used enema administration, characterized by smaller dose and higher localized concentration in the lesion, to improve the above situation.

We aimed to confirm that enema administration is a better modality than oral administration for GE against UC and to explore its mechanism.

We established UC mouse model, monitoring Disease Activity Index (DAI), inflammatory cytokines levels, and histopathology. Macrogenomics and bile acid (BAs) metabolomics analysed the major intestinal flora and BAs. Simultaneouslly, we conducted quantitative proteomics analysis and screened core proteins and pathway. In vitro validation was taken by qPCR, immunofluorescence and immunoblotting experiments.

GE via enema alleviate UC by inhibiting inflammatory factor production through downregulating S100A8/S100A9/NF-κB pathway. Analysis of the intestinal flora and BAs revealed that the enhanced abundance of Lachnospiraceae, which improves the ratio of primary to secondary BAs, and the reduced abundance of Provocaceae, which increases intestinal permeability and promotes inflammation, favored the restoration of the intestinal barrier. In addition, in vitro experiments confirmed that the key BA metabolites (mainly UDCA, DCA, and LCA) stimulated TGR5 signal to inhibit the assembly of the NLRP3 inflammasome and alleviated inflammation.

We firstly confirmed that GE alleviates UC via the enema route in a better manner than the oral route, through enhancing the intestinal barrier, restoring intestinal flora and BAs homeostasis, and inhibiting inflammatory injury. This study initially revealed that GE can alleviate UC through elevating UDCA, DCA, and LCA levels at the colonic site to activate TGR5 receptor for inhibiting the NLRP3 inflammasome, in addition to downregulating the S100A8/S100A9/-TLR4-NF-κB pathway related inflammatory response directly. The evidences offer a promising strategy and profround meaning for UC treatment.

The treatment of ulcerative colitis (UC) remains a huge challenge worldwide. Dictamnine is a natural product derived from Dictamnus dasycarpus Turcz. root bark and possesses multi-pharmacological properties, including anti-inflammation effects. However, its protective effect on UC and its underlying mechanisms are unknown.

Here we explored the protective effect and underlying mechanism of dictamnine against dextran sulfate sodium (DSS)-induced colitis in mice.

The experimental colitis was established by adding 3% DSS on drinking water of mice and the effects of dictamnine (10, 20, 40 mg/kg, p.o, once a day by 10 days) in colon tissues was analyzed. NCM460 cell was induced by RSL3 to detect the effect of dictamnine on ferroptosis and the underlying mechanism. Pathological damage was determined by H&E. Indicators related to intestinal permeability were detected by FITC and immunofluorescence. Cytokines levels (TNF-α、IL-1β and IL-6), antioxidant enzymes activities (MDA and GSH), the level of Fe2+ Cytokines levels and Gpx4 activity were detected by ELISA. Finally, the activation of nuclear factor erythroid 2-like 2 (Nrf2) was detected to explore the mechanism.

The results indicated that dictamnine significantly attenuated DSS-induced colon pathological damage, intestinal barrier, cytokines levels, and increased the antioxidant enzymes activities. Moreover, dictamnine attenuated ferroptosis in DSS-induced colon injury and upregulated Gpx4 expression in DSS-induced mice. Mechanistic experiments revealed that dictamnine activated Nrf2 in mice.

Taken together, this study evaluates that dictamnine alleviates DSS-induced colitis mice by inhibiting ferroptosis of enterocytes and its protective effects are associated with activating the Nrf2-Gpx4 signaling pathway.

Ulcerative colitis (UC) is a chronic inflammatory bowel disease in the colon and rectum. Mesenchymal stem cell-derived extracellular vesicles (MSCs-EVs) have emerged as promising cell-free therapeutics for UC, leveraging their immunomodulatory and tissue-protective properties. However, the specific epigenetic mechanisms by which EVs regulate pyroptosis (an inflammatory cell death pathway) remain poorly understood. This study explores how EVs derived from induced pluripotent stem cell-derived mesenchymal stem cells (iPSC-MSCs) regulate pyroptosis in colonic epithelial cells of UC by targeting the histone-modifying protein KDM6B, aiming to provide new therapeutic insights for UC. iPSCs were differentiated into MSCs, and their EVs were isolated and characterized. EVs were engineered to carry the circular RNA circ-CCND1 and co-cultured with UC model cells induced by DSS. Cell viability, inflammatory cytokine levels, and key molecular markers related to pyroptosis (NLRP3, cleaved Caspase-1, GSDMD-N) were measured. The molecular mechanism was dissected using RNA-protein binding assays and gene expression analysis, focusing on the circ-CCND1/KDM6B/ELF3/miR-342-3p signaling axis. EV treatment reduced pyroptosis in UC model cells, with enhanced efficacy when EVs carried circ-CCND1. Mechanistically, circ-CCND1 in EVs entered cells and bound to KDM6B, inhibiting its activation of the ELF3 gene, leading to increased miR-342-3p, which in turn suppressed KDM6B expression, forming a feedback loop that dampened pyroptosis. In conclusions, iPSC-MSC-derived EVs inhibit inflammatory cell death in colonic epithelial cells by regulating histone modification-related pathways, highlighting their potential as a novel therapeutic strategy for UC.

Disruption of intestinal epithelial integrity and increased permeability is central to the pathogenesis of ulcerative colitis (UC). In this study, we identified 3-aminobenzoic acid (3-ABA), a dietary component abundant in azuki beans, soybeans, and chickpeas as a regulator of epithelial permeability and inflammation in the colon. Screening 119 gut microbial metabolites revealed the ability of 4-ABA, a structural isomer of 3-ABA, to enhance barrier function in Caco2 cells. Further analysis of structural isomers identified 3-ABA as the most effective, significantly increasing transepithelial electrical resistance and reducing epithelial permeability. Using liquid chromatography-mass spectrometry, 3-ABA was detected in dietary beans and human fecal samples. Fecal 3-ABA levels were significantly lower in patients with UC compared with healthy individuals. Metagenomic and functional prediction analyses revealed dysbiosis in patients with UC, characterized by an enrichment of bacterial genes involved in ABA degradation. Gene expression analysis of 3-ABA-stimulated Caco2 cells demonstrated upregulation of tight junction molecules, such as CLDN1 and TJP1, enhancing epithelial barrier integrity. In a dextran sodium sulfate-induced colitis mouse model, rectal 3-ABA administration ameliorated colitis by enhancing epithelial barrier function and reducing inflammation. These findings highlight 3-ABA's potential as a dietary therapeutic agent for UC, offering a novel strategy to enhance intestinal integrity and mitigate inflammation.NEW & NOTEWORTHY Increased intestinal epithelial permeability is central to the pathogenesis of ulcerative colitis (UC). 3-Aminobenzoic acid (3-ABA), a dietary component abundant in beans, decreased epithelial permeability and attenuated colonic inflammation in a mouse experimental colitis model. Reduced fecal 3-ABA levels in patients with UC were associated with dysbiosis-driven accelerated degradation. These findings highlight the therapeutic potential of 3-ABA in UC by targeting colonic epithelium.

Ulcerative colitis is an idiopathic and chronic inflammatory bowel disease, characterized by inflammation of the mucosa of the colon and rectum. Clinical manifestations commonly include abdominal pain, diarrhea (with or without hematochezia), and weight loss. The pathogenesis of ulcerative colitis is multifactorial, involving a combination of genetic predispositions and lifestyle factors. High consumption of processed food, sedentary habits, alcohol intake, and stress are among the lifestyle factors implicated in disease onset and progression. Current treatment strategies focus on managing symptoms and inducing remission, however, the chronic nature of the disease, along with the adverse effects of conventional therapies, often compromises patient's quality of life. Therefore, exploring alternative therapies that can prolong remission and reduce symptom burden is important. Experimental evidence suggests that probiotics may extend remission duration in ulcerative colitis. Moreover, probiotics exhibit efficacy in amelioration clinical symptoms by reducing inflammation markers, preserving, and restoring intestinal epithelial. This review explores the advantages of the administration of probiotics in the treatment of ulcerative colitis, elucidating their mechanism of action.

Environmental factors, including poor dietary habits and unhealthy drinking patterns, contribute to ulcerative colitis (UC). While the relationship between diet-related malnutrition and UC has been extensively explored, the impact of drinking water temperature remains largely overlooked, prompting us to investigate its influence on UC pathogenesis and explore the underlying mechanisms. In the present study, we observed that, unlike external thermal and cold therapy, varying drinking water temperatures transiently altered the internal body temperature of the digestive tract. Specifically, chronic drinking of 0°C water had significant anti-inflammatory effects and preserved the integrity of the mucosal barrier in a colitis mouse model. Mechanistically, this temperature spectrum changed the composition of the gut microbiota from inflammation-prone (25°C drinking water) to a resting pattern similar to that of the negative control. Specifically, the abundances of Blautia and Parasutterella, two beneficial genera, were strongly increased in response to 0°C water, accompanied by elevated levels of short-chain fatty acids. In contrast, drinking 40°C water had opposite effects on all the examined parameters and generally aggravated the development of colitis. This study is the first to demonstrate how modifying the temperature of habitual drinking water can modulate colitis progression, providing a novel and noninvasive approach to UC management. Specifically, chronic consumption of 0°C water alleviated the severity of colitis, whereas 40°C water aggravated the disease. Therefore, by focusing on commonly consumed drinking water temperatures, our findings suggest that this simple intervention could be a safe, convenient, and effective therapeutic strategy.

Ulcerative colitis (UC) is an inflammatory bowel disease with an unknown cause. Previous studies have shown that Group 3 innate lymphoid cells (ILC3s) are crucial for maintaining intestinal mucosal immune homeostasis by producing key cytokines such as IL-22 and IL-17 A. While the RNA-binding protein Musashi-2 (MSI2) is recognized as essential for promoting intestinal epithelial regeneration post-injury, its impact on immune regulation remains unclear. Therefore, we aim to investigate the protective mechanisms associated with ILC3s-specific MSI2 deletion in a mouse model of ulcerative colitis.

Dextran sulfate sodium (DSS) was used to induce a mouse colitis model. Colitis severity was evaluated through weight loss, diarrhea, fecal traits, colon length, and pathological scoring. Transcriptome sequencing was utilized to identify differentially expressed genes in colon tissues. Flow cytometry was employed to measure the quantity and functionality of ILC3s. Western blot was conducted to analyze protein expression, while real-time polymerase chain reaction and enzyme-linked immunosorbent assay were employed to quantify inflammatory factors. Additionally, immunofluorescence, AB-PAS staining, and immunohistochemistry were employed to evaluate the integrity of the intestinal barrier.

Following DSS treatment, colon damage was milder in Msi2∆Rorc mice than in Msi2fl/fl mice. Transcriptomic analysis revealed the down-regulation of cytokines and pro-inflammatory factors in the colon tissue of Msi2∆Rorc mice. Flow cytometry showed that specific deletion of MSI2 reduced the infiltration of ILC3s in the intestinal lamina propria of Msi2∆Rorc mice and decreased IL-17 A production. The reduction of IL-17 A-mediated immune responses lessened inflammatory damage to the intestinal barrier, thereby reducing colitis severity.

Specific deletion of MSI2 alleviates DSS-induced colitis in mice by reducing ILC3s infiltration and IL-17 A secretion in the lamina propria of the colon. This decrease in inflammatory mediators and cell infiltration dampens the inflammatory response in the intestinal mucosa, helping to maintain the integrity of the intestinal barrier in mice with colitis. These findings enhance our understanding of UC pathogenesis and offer novel avenues for clinical diagnosis and treatment.

The association between vascular cell adhesion molecule-1 (VCAM-1) expression and intestinal mucosal inflammation and between VCAM-1 expression and the clinical course in patients with ulcerative colitis (UC) remains unclear. Therefore, we investigated not only the association between mucosal VCAM-1 expression and mucosal inflammation but also its association with subsequent relapse in UC patients with clinical remission.

Fifty-eight patients with UC in clinical remission and 16 patients in clinical active who visited Kyoto Prefectural University of Medicine for a 2-year follow-up period were included. VCAM-1 expression was compared between patients who subsequently relapsed and those who remained in remission, and it was examined in relation to endoscopic findings, histological activity, and cytokine expression. We also investigated the expression of mucosal addressin cell adhesion molecule-1 (MAdCAM-1).

VCAM-1 was associated with clinical disease activity and endoscopic severity and was significantly elevated in histologically active mucosa compared with inactive mucosa. VCAM-1 expression co-localized with MAdCAM-1 in the mucosal and submucosal microvessels of the colon and was significantly higher in the relapse group than in the remission group. Similar results were observed for MAdCAM-1 expression. VCAM-1 expression levels were also closely correlated with those of several other cytokines.

VCAM-1 expression in the colonic mucosa of patients with UC is associated with mucosal inflammation and subsequent relapse. These results suggest that VCAM-1 may serve as a marker for relapse and therapeutic effectiveness in UC, and that treatment targeting α4 integrin is efficient and rational.

This study aimed to analyze the advantageous effects of the decoction aqueous extract of Arbutus unedo fruits (AUFDE) against ulcerative colitis (UC) caused by acetic acid (AA) in rats, along with the processes involved in this protective effect. Adult male Wistar rats were divided into six groups: control (H2O), AA, AA combined with various doses of AUFDE (75, 150, and 300 mg kg-1 b.w., p.o.), and AA combined with sulfasalazine (SULF) (100 mg kg-1 b.w., p.o.) during 7 days. All rats underwent overnight fasting, followed by the induction of UC via rectal infusion of AA (300 mg kg-1 b.w.) at a concentration of 3% (v/v), administered at a volume of 5 mL kg-1 b.w. for 30 s. The colon was resected and subjected to macroscopic examination to assess ulcerated areas and the ulcer index.

The in vivo assay's findings revealed that AUFDE pretreatment attenuates histological changes and significantly reduces colonic mucosa lesions caused by AA. Also, AUFDE reduced the oxidative state that AA caused in the colonic mucosa, as indicated by elevated malondialdehyde levels and the reduction of both enzymatic antioxidants such as superoxide dismutase, catalase, and glutathione peroxidase, and non-enzymatic antioxidants such as thiol groups. Furthermore, AUFDE pretreatment controlled the dysregulation of all intracellular mediators and significantly decreased inflammatory indicators like C-reactive protein and alkaline phosphatase levels, whereas AA intoxication raised iron and calcium levels in plasma. According to our findings, AUFDE may have protected rats from AA-induced colitis. © 2025 Society of Chemical Industry.

JiuLiWan (JLW), as a classic traditional Chinese medicine formula, has been clinically used against ulcerative colitis (UC). However, the exact mechanism of its therapeutic effect remains unclear. This study aims to explore and validate the main components and pharmacological mechanism of JLW in the treatment of UC through network pharmacology, molecular docking, and cell experiments. Network pharmacology analyses indicated a total of 107 main components and 286 core targets of JLW against UC. Pathway enrichment analysis demonstrated the involvement of PI3K-AKT, MAPK, Ras, Rap1, TNF, T cell receptor, HIF-1, C-type lectin receptor, VEGF, and Th17 cell differentiation signal pathways in the efficacy of the formula. The molecular docking results indicated that the prominent components (ailanthone (AIL), butylidenephthalide, honokiol, dehydrocostuslactone, ganoderic acid A, atractylenolide I, neokurarinol, glycyrrhetinic acid, palmatine, tangeretin, and bruceine A) could bind to core targets AKT1, P53, STAT3, c-JUN, and ERK1. Subsequently, AIL was used as a representative compound to conduct cell experiments to verify its role and mechanism in anti-inflammation and immunomodulation. Interestingly, AIL could switch Jurkat T cells into a quiescence state without activating the inflammatory and immune status. However, AIL could significantly decrease the levels of interleukin-2 (IL-2) and interferon-gamma (IFN-γ), as well as the expression of surface activation markers CD69 and CD25, in PMA/ionomycin-activated Jurkat T cells by suppressing the RAF/ERK/STAT3 signaling pathway and increasing the phosphorylation of p53. This study combines network pharmacology prediction with experimental verification in vitro to demonstrate the mechanism of JLW in treating UC and provides an effective, safe, and inexpensive strategy for UC treatment.

Ulcerative colitis (UC) is a chronic inflammatory bowel disease, with untreated cases often progressing to colorectal cancer. Current treatments aim to induce inflammatory remission but often neglect the surrounding microenvironment, which significantly impairs mucosal healing and contributes to treatment failures. This study presents a novel silk fibroin-based fucoidan (SFU) in situ rectal gel, with sol-gel transition confirmed through rheological analysis under physiological pH and temperature conditions. The SFU gel exhibits strong antioxidant activity, achieving a DPPH radical scavenging rate of 73.3 ± 1.52%. The gel efficiently reduces reactive oxygen species (ROS) and nitric oxide (NO) production, demonstrating its reliable antioxidant effects. In a DSS-induced UC mouse model, SFU effectively alleviates colitis symptoms, including weight loss and disease activity index (DAI) reduction, with improved stool consistency and reduced rectal bleeding. Moreover, SFU therapy reprograms macrophages from proinflammatory M1 to anti-inflammatory M2 phenotypes, significantly lowering IL-6 and TNF-α levels, suggesting anti-inflammatory properties. Furthermore, SFU increased tight junction proteins Occludin-1 and ZO-1, indicating gut mucosal barrier integrity. SFU treatment restores goblet cells and mucin production while preventing fibrosis, demonstrating its potential as a natural therapy for UC treatment.

Inflammatory bowel disease (IBD) is a chronic and relapsing disease of the gastrointestinal tract. At present, antioxidant therapy is a promising strategy for IBD treatment. Since low-molecular-weight antioxidants (e.g., 2,2,6,6-tetramethylpiperidin-N-oxyl (TEMPO)) have a short in vivo half-life and inadequate cellular uptake, researchers have focused on loading antioxidants into nanostructures for improving their antioxidant and anti-inflammatory activities. As we know, in situ self-assembly with the formation of nanostructures under intracellular specific stimuli is a convenient delivery strategy to enhance the accumulation and retention of molecules at target sites in vivo. Herein, we developed an in situ self-assembled TEMPO probe TPP-FFYp-O to improve the antioxidant and anti-inflammatory effects of TEMPO in IBD. Compared to the control probe TPP-O without a self-assembly moiety, TPP-FFYp-O could successfully self-assemble into nanoparticles (NPs) under alkaline phosphatase (ALP)-guided dephosphorylation, with significantly enhanced antioxidant capacity in vitro. Cell experiments confirmed that intracellular formation of NPs by TPP-FFYp-O could improve the antioxidant and anti-inflammatory abilities of TEMPO and alleviate cellular damage. Moreover, TPP-FFYp-O exhibited good biocompatibility in vivo and significantly relieved pathological injury and inflammatory factors in the colon tissues of an IBD model compared to TPP-O. We envision that the in situ self-assembly platform can be used to load various active molecules for more applications in the future.

Systemic lupus erythematosus (SLE) and ulcerative colitis (UC) are both chronic autoimmune diseases with unclear shared mechanisms, largely due to limited mechanistic studies and clinical research cohorts. Transcriptome datasets from the Gene Expression Omnibus (GEO) database were analyzed for SLE and UC, identifying differentially expressed genes (DEGs). Weighted gene co-expression network analysis (WGCNA) identified significant module genes, including PLEKHA1. The diagnostic potential of PLEKHA1 was confirmed using machine-learning algorithms and real-time fluorescence quantitative PCR (RT-PCR) in clinical samples. Additionally, the study explored the link between PLEKHA1 and neutrophil extracellular trap (NET) formation. Our analyses identified transcriptional signatures associated with neutrophil degranulation and NET formation pathways in the peripheral blood of both SLE and UC, a perspective not previously explored. PLEKHA1 was identified as a promising biomarker that may impact NET formation. Pathway enrichment analyses indicated that PLEKHA1 plays a regulatory role in NET formation in both diseases. This study provides novel transcriptional evidence by proposing neutrophil degranulation and NET formation as common pathways in SLE and UC, with PLEKHA1 acting as a shared diagnostic gene. PLEKHA1 may regulate neutrophil activation and immune response, influencing NET formation and neutrophil degranulation in SLE patients' peripheral blood.

Lithospermic acid (LA), a plant-derived polycyclic phenolic carboxylic acid, is known for its strong anti-inflammatory and antioxidant effects. However, its effects have not yet been studied in ulcerative colitis (UC). This study aimed to assess the protective effects of LA in UC and investigate its potential mechanisms of action. Our findings indicated that LA effectively mitigated oxidative stress in mice with colitis by increasing the production of antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-PX), while reducing the levels of malondialdehyde (MDA) and reactive oxygen species (ROS) (p < 0.05 for all). In NCM460 cells, LA inhibited the Lipopolysaccharide (LPS)-induced increase in ROS and preserved the mitochondrial membrane potential. In vitro and in vivo experiments confirmed that LA decreased the production of inflammatory markers (p < 0.05). Additionally, LA upregulated intestinal mucosal proteins, contributing to mucosal barrier repair. Mechanistically, LA activated the nuclear factor erythroid 2-related factor 2 (Nrf2) signalling pathway, increasing the expression of Nrf2, heme oxygenase-1 (HO-1), and NAD(P)H quinone oxidoreductase 1 (NQO1) while inhibiting nuclear factor kappa B (NF-κB) phosphorylation (p < 0.05). Notably, the inhibition of Nrf2 reversed the protective effects of LA against colitis. Molecular docking analyses support a strong interaction between Nrf2 and LA. LA mitigates colitis-related inflammation and oxidative stress mainly by activating the Nrf2 signalling pathway. These findings support the potential development of LA as a novel therapeutic agent for UC.

Developing oral drug delivery systems is promising for ulcerative colitis (UC). However, the key challenges, including formulation degradation under harsh gastric conditions, poor targeting efficiency, and limited colonic residence, lead to poor therapeutic efficacy that still needs to be tackled. Effective treatment requires a safe, efficacious, enzyme- and pH-responsive, biomucoadhesive oral drug delivery system to overcome these challenges. Therefore, we have developed chitosan-armored 1,2-dimyristoyl-sn-glycero-3-phosphoglycerol (DMPG) nanoliposomes amalgamated with synthesized beta-sitosterol-sinapic acid (Be-S) conjugate, further encapsulated with 3,4-methylenedioxy-β-nitrostyrene (MNS) as NLRP3 inhibitor, termed C@MN@DMBe-S, to overcome the limitation of free MNS and sinapic acid. Formulated by the thin-film hydration method and processed through extrusion, these unilamellar liposomes demonstrated structural stability and mucoadhesive properties due to chitosan coating. This configuration protected the nanoliposomes from the gastric acidic environment and allowed retention in the inflamed colon for 48 h. The enzyme-responsive C@MN@DMBe-S nanoliposome releases sinapic acid at the inflamed colonic site via esterase activity, providing sustained and controlled release of MNS. This synergistic action delivers antioxidant and anti-inflammatory effects while influencing the gut microbiota composition by releasing short-chain fatty acids. Moreover, therapeutic investigations revealed that C@MN@DMBe-S exhibited superior efficacy compared with free MNS when administered orally. The formulation effectively downregulated NF-κB, NLRP3, Caspase-1, and IL-1β expression while upregulating MUC5AC expression, indicating enhanced anti-inflammatory and protective effects and thereby promoting mucosal healing. In addition, C@MN@DMBe-S was found to regulate immune cell expression and effectively downregulate neutrophil infiltration. This armor- and enzyme-responsive strategy elucidates the impact of oral nanomedicines on mitigating UC and is demonstrated as an effective treatment.

Ulcerative colitis (UC) is a non-specific inflammatory bowel disease. Unlike any single form of cell death reported previously, macrophage PANoptosis, a unique programmed cell death characterized by inflammation and necrosis, plays a crucial role in the pathogenesis of colitis. Changdiqing Decoction (CDQD), an empirical hospital prescription enema, has been used to treat UC for decades. This study aimed to investigate the multi-target anti-colitic effects of CDQD by examining its impact on intestinal homeostasis and its anti-inflammatory properties.

A dextran sulfate sodium (DSS)-induced mouse model of acute colitis was employed. Interferon-gamma (IFN-γ) and KPT-330 were used to induce macrophage PANoptosis. Ultra-high-performance liquid chromatography-high-resolution mass spectrometry (UHPLCHRMS) was utilized to identify the chemical constituents of CDQD. Multi-omics analysis and fecal microbiota transplantation (FMT) were used to explore the therapeutic targets and gut microbiota alterations induced by CDQD.

CDQD treatment significantly alleviated colitis symptoms in mice, with a dose-dependent therapeutic effect. The decoction mitigated PANoptosis in colon tissues and bone marrow-derived macrophages (BMDMs). 16S rRNA sequencing analysis and metabonomics revealed that CDQD administration significantly altered the gut microbiota composition and metabolite profiles. Notably, CDQD-modulated gut microbiota exhibited anti-colitic effects through FMT. Integrated transcriptomics and network pharmacology analysis revealed that CDQD significantly downregulated the PI3K/Akt signaling pathway in colitis. This finding was further validated using the inhibitors LY294002 and MK2206.

CDQD alleviates colitis by suppressing inflammatory macrophage activation and modulating the gut microbiota. Our research provides a novel traditional Chinese medicine strategy for the treatment of UC via enema administration.

Cuproptosis represents a novel mechanism of cellular demise characterized by the intracellular buildup of copper ions. Unlike other cell death mechanisms, its distinct process has drawn considerable interest for its promising applications in managing inflammatory bowel disease (IBD) and colorectal cancer (CRC). Emerging evidence indicates that copper metabolism and cuproptosis may exert dual regulatory effects within pathological cellular environments, specifically modulating oxidative stress responses, metabolic reprogramming, and immunotherapeutic efficacy. An appropriate level of copper may promote disease progression and exert synergistic effects, but exceeding a certain threshold, copper can inhibit disease development by inducing cuproptosis in pathological cells. This makes abnormal copper levels a potential new therapeutic target for IBD and CRC. This review emphasizes the dual function of copper metabolism and cuproptosis in the progression of IBD and CRC, while also exploring the potential application of copper-based therapies in disease treatment. The analysis further delineates the modulatory influence of tumor immune microenvironment on cuproptosis dynamics, while establishing the therapeutic potential of cuproptosis-targeted strategies in circumventing resistance to both conventional chemotherapeutic agents and emerging immunotherapies. This provides new research directions for the development of future cuproptosis inducers. Finally, this article discusses the latest advances in potential molecular targets of cuproptosis and their related genes in the treatment of IBD and CRC, highlighting future research priorities and unresolved issues.

This study investigates the effect and underlying mechanism of targeting SLC7A11 in mitigating dextran sulfate sodium (DSS)-induced intestinal inflammation and injury in colitis.

We utilized wild-type and SLC7A11-/+ mice to assess the inflammatory damage in DSS-induced colitis in vivo. In vitro, colon tissues from patients with ulcerative colitis were analyzed to compare SLC7A11 expression between inflamed and non-inflamed regions. Further mechanistic insights were obtained using Caco-2 cells and bone marrow-derived dendritic cells (BMDCs).

In human colon tissues, SLC7A11 expression was significantly elevated in inflamed regions compared to non-inflamed areas, particularly in dendritic cells. In vivo inhibition of SLC7A11 markedly alleviated DSS-induced colitis symptoms. In vitro, suppressing SLC7A11 restored the integrity of the Caco-2 monolayer intestinal epithelial model. Both knockout and inhibition of SLC7A11 enhanced ERK1/2 phosphorylation and increased efferocytosis in BMDCs.

Targeting SLC7A11 augments dendritic cell efferocytosis and preserves intestinal epithelial barrier function, potentially offering a therapeutic avenue for alleviating ulcerative colitis.

Ulcerative colitis (UC), a chronic relapsing-remitting inflammatory bowel disease. Recent studies have shown that lactylation modifications may be involved in metabolic-immune interactions in intestinal inflammation through epigenetic regulation, but their specific mechanisms in UC still require in-depth validation.

We conducted comparative analyses of transcriptomic profiles, immune landscapes, and functional pathways between UC and normal cohorts. Lactylation-related differentially expressed genes were subjected to enrichment analysis to delineate their mechanistic roles in UC. Through machine learning algorithms, the diagnostic model was established. Further elucidating the mechanisms and regulatory network of the model gene in UC were GSVA, immunological correlation analysis, transcription factor prediction, immunofluorescence, and single-cell analysis. Lastly, the CMap database and molecular docking technology were used to investigate possible treatment drugs for UC.

Twenty-two lactylation-related differentially expressed genes were identified, predominantly enriched in actin cytoskeleton organization and JAK-STAT signaling. By utilizing machine learning methods, 3 model genes (S100A11, IFI16, and HSDL2) were identified. ROC curves from the train and test cohorts illustrate the superior diagnostic value of our model. Further comprehensive bioinformatics analyses revealed that these three core genes may be involved in the development of UC by regulating the metabolic and immune microenvironment. Finally, regorafenib and R-428 were considered as possible agents for the treatment of UC.

This study offers a novel strategy to early UC diagnosis and treatment by thoroughly characterizing lactylation modifications in UC.

Colitis is a multifactorial inflammatory bowel disease (IBD) involving intestinal barrier dysfunction, immune dysregulation, oxidative stress, and microbiota imbalance. Lactobacillus salivarius (L. salivarius), a probiotic with antioxidative and anti-inflammatory properties, was evaluated in a mouse model of DSS-induced colitis. Treatment with L. salivarius significantly reduced weight loss, colon shortening, and disease activity index, while improving histopathological damage. DSS-induced colitis exhibited significant oxidative stress, evidenced by decreased total antioxidant capacity, increased malondialdehyde (MDA), and reduced activity of antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). After the intervention of L. salivarius, MDA levels in colon tissues decreased significantly, while SOD and GSH-Px activities increased significantly. In DSS-induced colitis models, the expression of pro-inflammatory cytokines (such as TNF-α, IL-6, IL-1β) was significantly increased, while the expression of anti-inflammatory cytokine IL-10 was decreased. After the intervention of L. salivarius, the level of proinflammatory factors was significantly down-regulated, while the level of IL-10 was up-regulated. DSS treatment leads to a significant imbalance in the intestinal microbiota, characterized by an increase in the ratio of Firmicutes to Bacteroidetes (F/B ratio). The abundance of pathogenic bacteria (Alistipes, Candidatus_Soleaferrea, Frisingicoccus, Romboutsia, Streptococcus) increased, while beneficial bacteria (Anaerotruncus, Rikenella) decreased. After probiotic administration, the F/B ratio was restored significantly, and the abundance of important beneficial bacteria increased while the abundance of pathogenic bacteria decreased. These results suggest that L. salivarius alleviates DSS-induced colitis by enhancing antioxidant defense, regulating inflammatory responses, and restoring gut microbiota balance. This probiotic may offer a promising therapeutic strategy for managing ulcerative colitis (UC).

Inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, is characterized by chronic intestinal inflammation and impaired epithelial barrier function. Emerging evidence highlights the critical role of vascular remodeling and angiogenesis in IBD pathogenesis. This review explores the intricate relationship between blood vessels and the intestinal epithelial barrier, emphasizing how aberrant vascularization contributes to barrier dysfunction and disease progression. In IBD, excessive angiogenesis is driven by hypoxia, immune cell infiltration, and pro-inflammatory cytokines, further perpetuating inflammation and tissue damage. Key angiogenic factors, such as vascular endothelial growth factor (VEGF), angiopoietins, and platelet-derived growth factor (PDGF), are upregulated in IBD, promoting pathological vessel formation. These newly formed vessels are often immature and hyperpermeable, exacerbating leukocyte recruitment and inflammatory responses. Given the pivotal role of angiogenesis in IBD, anti-angiogenic therapies have emerged as a potential therapeutic strategy. Preclinical and clinical studies targeting VEGF and other angiogenic pathways have shown promise in reducing inflammation and promoting mucosal healing. This review summarizes current knowledge on vascular-epithelial interactions in IBD, the mechanisms driving pathological angiogenesis, and the therapeutic potential of anti-angiogenic approaches, providing insights for future research and treatment development.

Inflammatory bowel disease (IBD) is an inflammatory disease of the intestine whose primary pathological presentation is the destruction of the intestinal epithelium. The intestinal epithelium, located between the lumen and lamina propria, transmits luminal microbial signals to the immune cells in the lamina propria, which also modulate the intestinal epithelium. In IBD patients, intestinal epithelial cells (IECs) die dysfunction and the mucosal barrier is disrupted, leading to the recruitment of immune cells and the release of cytokines. In this review, we describe the structure and functions of the intestinal epithelium and mucosal barrier in the physiological state and under IBD conditions, as well as the patterns of epithelial cell death and how immune cells modulate the intestinal epithelium providing a reference for clinical research and drug development of IBD. In addition, according to the targeting of epithelial apoptosis and necroptotic pathways and the regulation of immune cells, we summarized some new methods for the treatment of IBD, such as necroptosis inhibitors, microbiome regulation, which provide potential ideas for the treatment of IBD. This review also describes the potential for integrating AI-driven approaches into innovation in IBD treatments.

Emerging data indicate a stabilizing incidence of inflammatory bowel diseases (IBD), including ulcerative colitis (UC), Crohn's disease (CD), and IBD unclassified (IBDU) in Western countries. We aimed to investigate the incidence of IBD, its initial clinical presentation, and patient-reported burden.

Copenhagen IBD Inception Cohort is a prospective, population-based cohort of patients with newly diagnosed IBD according to the ECCO guidelines in the period between May 2021 and May 2023, within a catchment area covering 20% of the Danish population.

Based on 554 patients (UC: 308, CD: 201, and IBDU: 18), the incidence rates per 100 000 person-years were as follows: IBD: 23.4 (95% confidence interval, 21.5-25.4), UC: 14.0 (12.6-15.6), CD: 8.6 (7.4-9.8), and IBDU: 0.8 (0.5-1.3). The median diagnostic delay was significantly shorter for UC (2.5 months [interquartile range {IQR} 1-6]) than for CD (5 months [IQR 1.5-11], p < 0.01). Moderate-to-severe disability was reported by 34% of CD patients and 22% of UC patients (p = 0.01), severe fatigue by 30% and 26% (p = 0.43), and severely impaired health-related quality of life (HRQoL) by 43% and 30% of patients, respectively (p = 0.01). Hospitalization rates (UC: 20%, CD: 34%, p < 0.01), and need for immunomodulators, biologics, or surgery within 3 months of diagnosis, were high in both UC (3%, 7%, and 37%, respectively) and CD (31%, 18%, and 10%, respectively).

We found a high incidence of IBD in Copenhagen with a substantial disease burden characterized by early and high requirements for advanced therapies and high rates of fatigue, disability, and impaired HRQoL at diagnosis.

The diagnostic and prognostic properties of anti-integrin αvβ6 immunoglobulin G (IgG) autoantibodies in ulcerative colitis (UC) are poorly understood. We aimed to assess the diagnostic performance of anti-integrin αvβ6 autoantibodies and examine their association with disease outcomes.

Serum samples from a Swedish inception cohort of patients with suspected inflammatory bowel disease (IBD, n = 473) were analyzed using an in-house fluorescence enzyme immunoassay based on EliA technology. Findings were validated in a Norwegian population-based inception cohort (n = 570). Diagnostic performance was assessed by calculating the area under the curve (AUC) with 95% confidence intervals and determining sensitivity and specificity. Reclassification was evaluated using the net reclassification index.

In the discovery cohort, patients with UC, IBD-unclassified, or colonic Crohn's disease exhibited higher median autoantibody levels compared to symptomatic and healthy controls. In the validation cohort, the autoantibody demonstrated 79% sensitivity and 94% specificity for UC vs symptomatic controls at a cut-off of 400 UA/l. Its diagnostic performance (AUC = 0.92, 95% CI, 0.89-0.95) was superior to hs-CRP (AUC = 0.65, 95% CI, 0.60-0.70, P < .001) and faecal calprotectin (fcalpro) (AUC = 0.88, 95% CI, 0.84-0.92, P = .09). Combining the autoantibody with fcalpro further improved diagnostic accuracy (AUC = 0.97, 95% CI, 0.95-0.98) and patient reclassification (P < .001). Autoantibody positivity was associated with a severe phenotype of UC, characterised by increased inflammatory activity and higher IL-17A and granzyme B levels. Higher autoantibody levels were linked to an aggressive disease course, remaining stable in aggressive UC but decreasing in indolent disease (P = .003).

Anti-integrin αvβ6 is a reliable diagnostic and prognostic marker for UC, with potential clinical implementation.

Regulatory T cells (Tregs) are the principal immune cells that exert anti-inflammatory effects within the organism. Their exosomes exhibit therapeutic efficacy across a broad spectrum of diseases owing to their high stability, low immunogenicity, and substantial penetration capacity. Recent research have indicated that isoallolithocholic acid (isoalloLCA), a metabolite associated with bile acid metabolism, may enhance Treg activity by upregulating forkhead box protein3 (Foxp3) expression. Hence, metabolite-based strategies for reinforcing Tregs may offer novel intervention options for treating related diseases. In this study, tumor necrosis factor (TNF)-α and dextran sulfate sodium (DSS) were employed to establish cellular and animal models of inflammatory bowel disease (IBD), further evaluating the therapeutic efficacy of isoalloLCA-intervened regulatory T cell exosomes (isoalloLCA-Exo) within this model. Our findings demonstrated that isoalloLCA-Exo effectively inhibit colitis progression in a murine model, as indicated by reduced inflammation, decreased apoptosis of intestinal epithelial cells, and improved intestinal barrier function. Furthermore, in vitro analyses elucidated the molecular mechanisms underlying the anti-inflammatory effects of isoalloLCA-Exo, revealing that the intervention effectively reversed TNF-α-induced inflammation and apoptosis in intestinal epithelial cells by modulating the NF-κB pathway. In conclusion, isoalloLCA-Exo can decelerate inflammatory bowel disease progression and suppress inflammatory response in intestinal epithelial cells by inhibiting NF-κB pathway. Notably, isoalloLCA-Exo exhibit superior efficacy to the traditional drug mesalazine and conventional treg exosome(NC-Exo). These findings have significant implications for optimizing Treg-derived exosome-based therapies for inflammation-related diseases.

Ulcerative colitis (UC) is a chronic inflammatory bowel disease with a rising incidence globally, whereas existing treatments exhibit significant limitations. Coix seed polysaccharide (CSP), a component of traditional Chinese medicine known for its immunomodulatory and antioxidant properties, has not been thoroughly investigated for its role in UC. In this study, CSP was prepared via water extraction and ethanol precipitation, and its protective effects and mechanisms were evaluated using a dextran sulfate sodium salt (DSS)-induced UC mouse model. The results demonstrated that CSP significantly ameliorated DSS-induced UC symptoms, including weight loss, an elevated Disease Activity Index, colon shortening, increased levels of inflammatory cytokines, and intestinal barrier damage. Moreover, CSP reshaped the DSS-induced gut microbiota dysbiosis by increasing gut microbial diversity and regulating the abundance of specific genera, such as increasing Anaerotruncus. Metabolomic analysis revealed that CSP significantly modulated the levels of 116 metabolites, particularly enhancing the beneficial metabolite 3-hydroxybutyrate. Importantly, the preventive effect of CSP on UC was dependent on the gut microbiota and could be transferred via fecal microbiota transplantation. This study demonstrates that CSP, a microecology-regulating polysaccharide, effectively modulates gut microbiota and alleviates symptoms of UC. These findings support the potential of CSP as a dietary supplement for UC prevention and underscore its value in the development of medicinal foods and functional food applications.

This study explores the impact of Faecalibacterium longum CM04-06 on inflammatory bowel disease (IBD) by regulating gut microbiota in mice.

We reanalyzed the distribution of the CM04-06 genome in the metagenome of the IBD cohort and observed a significantly higher abundance of CM04-06 in healthy individuals compared to patients with UC or CD. The prophylactic administration of CM04-06 was evaluated for its effects on intestinal microbial diversity and community composition after a two-week trial in mice. The intestinal microbiota was characterized using metagenomic sequencing of fecal samples on the DNBSEQ platform. CM04-06 treatment resulted in a significant reduction in the Disease Activity Index (DAI) and histological scores, as well as a decrease in the levels of pro-inflammatory cytokines, including IL-1β, IL-6, and TNF-α, in both the colon and serum of DSS-induced mice. Furthermore, supplementation with CM04-06 significantly reduced the levels of pro-inflammatory cytokines in both the colon and serum. Additionally, CM04-06 enhanced the integrity of the intestinal epithelial barrier by increasing the expression of tight junction proteins and mucin. Moreover, we observed greater abundances of Faecalibaculum rodentium, Alistipes onderdonkii, Alistipes shahii, and Bifidobacterium animalis after CM04-06 treatment.

CM04-06 prevents and alleviates intestinal inflammation by modulating the composition of the microbiota community, increasing the abundance of beneficial probiotics, and suppressing pro-inflammatory cytokine levels.

Dysbiosis refers to the disruption of the gut microbiota balance and is the pathological basis of various diseases. The main pathogenic mechanisms include impaired intestinal mucosal barrier function, inflammation activation, immune dysregulation, and metabolic abnormalities. These mechanisms involve dysfunctions in the gut-brain axis, gut-liver axis, and others to cause broader effects. Although the association between diseases caused by dysbiosis has been extensively studied, many questions remain regarding the specific pathogenic mechanisms and treatment strategies. This review begins by examining the causes of gut microbiota dysbiosis and summarizes the potential mechanisms of representative diseases caused by microbiota imbalance. It integrates clinical evidence to explore preventive and therapeutic strategies targeting gut microbiota dysregulation, emphasizing the importance of understanding gut microbiota dysbiosis. Finally, we summarized the development of artificial intelligence (AI) in the gut microbiota research and suggested that it will play a critical role in future studies on gut dysbiosis. The research combining multiomics technologies and AI will further uncover the complex mechanisms of gut microbiota dysbiosis. It will drive the development of personalized treatment strategies.

Ulcerative colitis (UC) is characterized by abdominal pain and bloody diarrhoea and restoring the gut barrier is the core goal of UC treatment. Activation of aryl hydrocarbon receptor (Ahr) was reported to effectively alleviate symptoms and repair the gut barrier damage. Neutrophil extracellular traps (NETs) have been recognized as potential targets in the treatment of UC. Ahr activation has been found to be capable of upregulating Nqo1, thereby reducing the production of reactive oxygen species (ROS), which is important in the formation of NETs. Quercetin (QUE), which is derived from natural plants and herbs used in traditional Chinese medicine (TCM), is able to strengthen gut barrier function by activating Ahr.

The aim of this study is to investigate how QUE suppresses NETs in UC and activates Ahr in neutrophils.

In this study, the dextran sulfate sodium (DSS)-induced UC model was used. Histopathological assessments were performed in the paraffin slides of tissues after H&E, PAS, Masson and alcian blue staining. The concentration of cytokines was also detected using cytometric beads array kits. Based on the transcriptomic analysis of colon tissues, western blot (WB) analysis, immunohistochemistry (IHC) assays and immunofluorescence (IF) assays were conducted to validate the significantly regulated genes and pathways. In vitro, the binding of quercetin to Ahr was calculated by molecular dynamic simulations (MDS) and biolayer interferometry (BLI) analysis. Primary neutrophils isolated from mice were cocultured with LPS or PMA with or without quercetin. The regulated genes were detected using WB, real-time quantitative PCR, enzyme-linked immunosorbent assay (ELISA) and IF analysis. The agonists and antagonist of Ahr were used as the control.

After the administration of quercetin, colon inflammation and gut barrier disruption was significantly prevented through inhibiting the NF-κB pathway and upregulating the expression of Ahr/Arnt and Nqo1. The transcriptomic analysis and IHC assays showed that inflammation and NETs were greatly decreased by QUE treatment. In vitro, quercetin inhibited LPS-induced inflammatory responses through NF-κB pathway. Furthermore, MDS and BLI analysis revealed that QUE is an agonist of AHR. QUE activated Ahr translocation and reduced ROS production via regulation of Arnt and Nqo1.

This study proved that quercetin greatly improved gut barrier function in the DSS-induced colitis model by regulating NET formation and that quercetin was able to activate Ahr and upregulate Arnt in neutrophils to regulate NET formation.

Ulcerative Colitis (UC) is a chronic inflammatory condition resulting from an abnormal immune response to gut microbiota, leading to cytokine dysregulation, including elevated interleukin-23 (IL-23) levels. Emerging evidence suggests that vitamin D (VD) plays a crucial role in immune modulation. However, its correlation with IL-23 in UC is not well addressed. This study aims to elucidate the relationship between serum VD and IL-23 levels in UC patients. We included forty-four UC patients and forty-four healthy controls. VD insufficiency was more common in UC patients (n = 14) compared to controls (n = 5). Significant increases in IL-23 levels were observed from remission (46.6 ± 4.3 pg/mL) to severe stages (218.5 ± 62.41 pg/mL), while VD levels did not show a similar trend. IL-23 levels also rose significantly with disease extent, from proctitis to pancolitis. A significant negative correlation was found between VD and IL-23 levels (r = -0.3175; P = 0.035). IL-23 and pulse rate were significant predictors of UC in our cohort. Our findings highlight VD insufficiency to be prevalent in UC patients, with VD levels negatively correlating with IL-23 levels, which increase with disease severity and extent. Further, understanding the interplay between VD and IL-23 will help design therapeutic interventions to modulate immune response and disease progression.

Ulcerative colitis (UC) is a complex inflammatory condition with limited non-invasive tools to monitor early-stage inflammation. This study aimed to investigate the early stages of inflammation in acute and chronic murine models of dextran sulfate sodium (DSS)-induced colitis using in vivo and ex vivo chemiluminescence imaging.

Two DSS-induced colitis models were used: an acute model over 7 days and a chronic model over 6 weeks. Body weight, stool consistency, and fecal occult blood (FOB) tests were monitored. Chemiluminescence imaging was used to assess inflammation in vivo and ex vivo, complemented by colonoscopy in the chronic model.

In the acute model, DSS-treated mice exhibited weight loss, colon shortening, and positive FOB tests by day 7. Ex vivo chemiluminescence signals exhibited a significant increase as early as day 5 (p < 0.001), while in vivo imaging showed minimal changes. In the chronic model, periodic DSS exposure resulted in recurrent inflammation, with positive FOB tests and significantly elevated ex vivo and in vivo chemiluminescence signals during the final DSS cycle (p < 0.05). Colonoscopy confirmed inflammation progression.

This study demonstrates the progression of inflammation in acute and chronic colitis models. However, in vivo chemiluminescence imaging did not reliably detect the onset of inflammation, limiting its application for early-stage disease detection. Ex vivo chemiluminescence and FOB tests provided more consistent insights into inflammation dynamics, addressing the need for improved non-invasive monitoring tools in UC research.

The term alarmin denotes a broad class of molecules rapidly released to alert the immune system through the engagement of specific receptors on immune cells. Three alarmin cytokines-thymic stromal lymphopoietin, IL-33, and IL-25-are released from epithelial and certain stromal cells. TNF-like cytokine 1A (TL1A) is a member of the TNF cytokine superfamily, first identified in human endothelial cells. TL1A is now considered a novel alarmin expressed by human and mouse bronchial and intestinal epithelial cells. TL1A exerts its biological activities by binding to a trimeric receptor DR3 (death receptor 3), expressed on a wide spectrum of immune and structural cells, including lung fibroblasts, endothelial cells, and bronchial epithelial cells. TL1A has been implicated in experimental and human inflammatory bowel diseases as well as in airway inflammation and remodeling in severe asthma. A monoclonal antibody anti-TL1A (tulisokibart) is effective in inducing clinical remission in ulcerative colitis patients. Increasing evidence suggests that TL1A is also involved in certain autoimmune disorders, such as rheumatoid arthritis and psoriasis. These emerging findings broaden the role of TL1A in various human inflammatory conditions. Several clinical trials are currently evaluating the safety and efficacy of monoclonal antibodies targeting TL1A in asthma or inflammatory bowel disease patients.

Background and Objectives: The purpose of this study was to evaluate potential protective effects of suramin on inflammation, oxidative stress, and histopathological damage a rat model of acute colitis created with acetic acid. Materials and Methods: Wistar albino (male) rats were randomly assigned to three groups: control (n = 10), colitis + saline (n = 10), and colitis + suramin (n = 10). Rectal instillation of 4% acetic acid was used to induce acute colitis. Suramin (10 mg/kg/day) or saline was administered intraperitoneally for 15 days. Plasma concentrations of pentraxin 3 (PTX3), tumor necrosis factor-alpha (TNF-α), neutrophil extracellular traps (NETs), and malondialdehyde (MDA) were determined using enzyme-linked immunosorbent assay (ELISA) and spectrophotometric methods. In addition, vascular endothelial growth factor (VEGF) and TNF-α levels in colonic tissue were also measured. Histopathological evaluations were conducted using hematoxylin and eosin staining. Results: Significant increases in plasma and tissue inflammatory markers, oxidative stress parameters, and histopathological scores were observed when compared to control group; values were higher in colitis group. Suramin treatment significantly reduced plasma PTX3, TNF-α, NETs, and MDA levels, and colonic TNF-α and VEGF concentrations compared to the untreated colitis group. Histological analysis showed reduced epithelial injury and leukocyte presence in rats receiving suramin. Conclusions: Our findings demonstrate that suramin significantly attenuates inflammatory and oxidative damage in an experimental model of acute colitis. These results suggest that suramin may possess therapeutic potential in intestinal inflammation; however, this effect requires further support through advanced experimental and clinical studies.

The purpose of this study is to analyze the current research status and explore the relationship between metabolites and inflammatory bowel disease (IBD), providing insights for future research.

In this study, we retrieved publications on metabolites and IBD from the Web of Science Core Collection (WOSCC), covering the period from 1994 to 2024. We conducted descriptive and visual analyses of the topics, journals, countries/regions, institutions, authors, and citation counts of these publications.

From January 1994 to June 2024, a total of 509 relevant publications were retrieved from the WOSCC, with the number of publications steadily increasing each year. These articles were published in 222 journals, with the top three most productive journals being inflammatory bowel diseases (36 publications), Alimentary Pharmacology & Therapeutics (16 publications), and Digestive Diseases and Sciences (13 publications). The leading countries in publication output were China (154 publications, 30.3%), the USA (101 publications, 19.8%), and the UK (32 publications, 6.3%), with total citation counts of 3,175, 7,439, and 1,444, respectively. The most recent trending keywords in this field include "gut microbiota," "inflammation," and "pathogenesis."

Recent research on the relationship between metabolites and inflammatory bowel disease (IBD) has grown significantly, deepening our understanding of their connection. Further exploration of this relationship could not only enhance the quality of life for IBD patients but also offer new insights into potential cures for the disease.