Sevoflurane is a widely used inhalation anesthetic during the perioperative period. Recent studies have suggested that sevoflurane has an enteroprotective effect, but its mechanism is unclear. To explore the mechanism of sevoflurane in intestinal ischemia‒reperfusion injury, an intestinal ischemia‒reperfusion injury mouse model was established. First, intestinal ischemia‒reperfusion injury was compared between aged and young mice. The results showed that intestinal ischemia‒reperfusion injury caused pathological intestinal injury and disrupted the intestinal mucosal barrier. The aged mice had more severe intestinal ischemia‒reperfusion injury than the young mice and therefore had a lower survival rate. The aged mice subsequently received sevoflurane via inhalation. Sevoflurane alleviated the pathological injury to the intestinal mucosa and repaired the function of the intestinal mucosal barrier in aged mice, thus increasing the level of intestinal mucosal hypoxia-inducible factor-1α and improving the survival rate of aged mice. However, preoperative administration of the hypoxia-inducible factor-1α inhibitor BAY87-2243 could counteract the enteroprotective effect of sevoflurane and lower the expression level of heme oxygenase-1, a downstream antioxidant enzyme of hypoxia-inducible factor-1α. Our findings suggest that sevoflurane alleviates intestinal ischemia‒reperfusion injury in aged mice by repairing the intestinal mucosal barrier through the activation of hypoxia-inducible factor-1α/heme oxygenase-1, providing a new target for the treatment of intestinal ischemia‒reperfusion injury in aged mice.

This study investigated the preventive effects and mechanisms of Paeonia lactiflora pall stem and leaf extract (PLE) on oxidative stress-induced diarrhea in broilers, using a Diquat (DQ)-induced model. Results indicated that PLE significantly improved growth performance, increased average daily gain (ADG), reduced feed-to-gain ratio (F/G), and enhanced liver and kidney indices. PLE alleviated DQ-induced oxidative stress diarrhea by reducing the diarrhea rate by 63.84%, upregulating mRNA expression of MUC2, Claudin-1, ZO-1, and Occludin, and decreasing AST and ALT activities in serum. Additionally, PLE increased levels of CAT, SOD, GSH-Px, and GSH while reducing PCO and MDA levels in serum, intestine, and liver tissues. Furthermore, PLE increased acetic acid content and decreased propionic acid, butyric acid, and isobutyric acid contents. PLE also altered gut microbiota by up-regulated Bacteroidetes and Barnesiella and down-regulated Firmicutes and unclassified_o__Eubacteriales. Network pharmacology suggested that PLE acts via the PI3K-Akt-Nrf2 pathway, confirmed by up-regulated mRNA expression of PI3K, AKT, Nrf2, NQO1, and HO-1, and down-regulated Keap1 in intestinal and liver tissues. Correlation analysis revealed significant associations between Barnesiella and unclassified_o__Eubacteriales with short-chain fatty acids and PI3K-Akt-Nrf2 pathway-related genes. Thus, PLE prevents and alleviates oxidative stress-induced diarrhea in broilers by modulating the PI3K-Akt-Nrf2 pathway, regulating gut microbiota, and influencing short-chain fatty acids.

Nucleus pulposus cells (NPCs) undergo metabolic disorders and matrix pathological remodeling under the influence of various adverse factors during intervertebral disc degeneration (IVDD), whereas post-translational modifications (PTMs) can confer cells with the capacity to respond quickly and adapt to complex environmental changes. Here, SIRT1 protein, a key regulator within PTMs framework, was applied against the hostile degenerative microenvironment. Then, it was sequentially assembled with SOX9-expressing plasmid, an essential transcription factor to promote extracellular matrix (ECM) biosynthesis, onto a phenylboronic acid-functionalized G5-dendrimer to construct a multifunctional nanoplatform for IVDD therapy. In vitro, the nanoplatforms showed antioxidant capacity, and the ability to restore mitochondrial homeostasis and normal ECM metabolism, as well as to maintain cellular phenotypes. RNA sequencing suggested that inhibition of the Nod-like receptor signaling might be the mechanism behind their therapeutic effects. The nanoplatforms were then wrapped in a designed dynamic hydrogel, not only prolonging the retention time of the loaded cargoes, but also well maintaining the disc structure, height, and water content in vivo. Overall, this study presents a convenient assembled strategy to inhibit the multiple adverse factors, and hold promise for the IVDD treatment.

Prior research has revealed an association between smoking, reduced ulcerative colitis (UC) risk, and improved disease severity among individuals with existing UC. Herein, we analysed the interaction between smoking habits and UC and its potential complexity, focusing on associations between smoking, incidence of UC, and therapeutic outcomes, via a meta-analysis of data from case-control studies. The PubMed, China Knowledge, WanFang, Web of Science, China Science and Technology Journal, Embase, and Scopus databases were searched, yielding nine case-control studies investigating the association between smoking and UC progression for inclusion. Compared to non-smoking or smoking cessation, smoking had a protective effect against UC, indicating that it may reduce the risk of developing UC; specifically, smoking was associated with a significant protective effect against UC compared to smoking cessation (pooled odds ratio (OR): 0.26, 95% confidence interval (CI): 0.21-0.32; P = 0.067, I2 = 45.2%). Non-smoking was also protective compared with smoking cessation (pooled OR: 1.84, 95% CI 1.13-3.30; P = 0.935, I2 = 0%). Further, smoking was significantly more protective than non-smoking (pooled OR: 0.48, 95% CI 0.40-0.56; P = 0.002, I2 = 66.4%). These results indicate that smoking offers some protection against UC onset and may reduce disease severity in patients with existing UC.

Inorganic dietary nanoparticles (IDNPs) are frequently utilized as food additives and in packaging, resulting in their exposure becoming a substantial yet often overlooked concern for patients with inflammatory bowel disease (IBD). Considering that impaired intestinal barrier function plays a central role in the pathogenesis of IBD, this review concentrates on the roles and mechanisms of IDNPs in the intestinal barrier (physical, chemical, biological, and immune barriers) of IBD patients. Previous studies have shown that different types of nanoparticles have varying effects on animals in diverse states. In this context, factors such as the source, size, shape, dosage, and duration of action of the nanoparticles, as well as the species, gender, dietary habits, and age of the animals, significantly influence research outcomes. Future studies should undertake more comprehensive explorations into the effects and mechanisms of IDNPs with diverse sources and properties in IBD patients.

To investigate the role of gut microbiota in methotrexate (MTX)-induced gastrointestinal reactions (MRGR) in patients with rheumatoid arthritis (RA).

As a prospective, single-center, convenience sampling study, stool samples were obtained from 28 RA patients (male: female = 10:18) at Lanzhou University Second Hospital who were undergoing MTX treatment for analysis of their gut microbiota using 16S rRNA gene sequencing. Clinical disease activity (CDAI) and MRGR were assessed after two months of MTX therapy. All data collection periods exceeded one year. Intestinal germ-free mice, generated through antibiotic treatment, received fecal microbiota transplantation (FMT) from the patients, followed by varying doses of MTX to observe MRGR. Intestinal transcriptomics and markers related to intestinal barrier function were subsequently examined.

Females (84.6%) and high disease activity (CDAI scores, 39.6 ± 11.2 vs 26.3 ± 9.2) were prone to have MRGR in RA patients. Patients with MRGR (PT-GR) showed lower gut microbial diversity versus non-MRGR (PT-noGR). Prevotella abundance, positively correlated with CDAI and MRGR (p < 0.05), was elevated in PT-GR. Administering 10 mg/kg MTX to mice caused intestinal damage. FMT-GR-MTX mice exhibited weight loss (95.2%), morphological deterioration (86.4%), and reduced tight junction proteins (Claudin-1:72.4%; ZO-1:81.2%). Transcriptomics linked upregulated Gβγ/CREB/Atp4b to PI3K/Akt/Ras pathways and downregulated PFK2/PP2 to AMPK signaling in MRGR.

Our study identified notable gut microbiota alterations in RA patients prone to MRGR, with changes in intestinal gene expression and reduced intestinal barrier function potentially contributing to MRGR. These findings suggest potential strategies to mitigate MRGR in RA patients undergoing MTX treatment. Key Points • The RA-related MRGR is correlated with the intestinal microbiota. • Females, low gut diversity, and Prevotella enrichment are MRGR risks in RA. • Upregulated DEGs in MRGR linked to PI3K/Akt, Ras pathways. • Downregulated DEGs in MRGR focus on the AMPK pathway.

Apostichopus japonicus is one of the most popular types of sea cucumber among consumers in Southeast Asia. Fucoidan from Apostichopus japonicus (Aj-FUC) has attracted considerable attention because of its immunomodulatory activities. Aj-FUC is indigestible in the human upper gastrointestinal tract but can be utilized by the gut microbiota. Thus, we suspect that Aj-FUC interacts with the gut to enhance immunefunction. This study showed that after a three-week intervention with Aj-FUC (100 mg/kg/d), the gut microbiota in mice developed a new homeostasis. Subsequently, in the condition of intestinal flora homeostasis, the effects of Aj-FUC on intestinal health in normal mice and the prevention of intestinal mucosal damage in cyclophosphamide-induced mice were investigated. Aj-FUC preserved intestinal structural integrity, increased the number of goblet cells, upregulated the expression of ZO-1 and Occludin, stimulated the secretion of sIgA and IgA, and maintained the Th1/Th2 balance. Importantly, beneficial bacteria were enriched, and tryptophan metabolism-related metabolites such as 5-hydroxyindole-3-acetic acid, and indole-3-lactic acid were upregulated following Aj-FUC administration. In summary, a three-week Aj-FUC intervention could result in the formation of a new homeostasis in intestinal flora, while the effect of Aj-FUC on intestinal immunity was related to the regulation of tryptophan metabolism by gut microbiota.

Korean mistletoe (Viscum album var. coloratum, KML) offers remarkable therapeutic potential for a variety of diseases. This study aims to evaluate the effects and potential molecular mechanisms of KML ethanol extracts (KMLE), focusing on intestinal barrier function and tight junctions (TJs) in an interleukin (IL)-6-induced Caco-2 cell monolayer model and a dextran sodium sulfate (DSS)-induced ulcerative colitis (UC) mouse model. KMLE is non-cytotoxic in Caco-2 cells and demonstrated strong antioxidant activity. KMLE alleviated significant barrier dysfunction and protected tight junction proteins (TJPs) in vitro. Furthermore, KMLE alleviated clinical symptoms and histopathological damage, upregulated TJPs, and suppressed the inflammatory cytokines in vivo. Additionally, six bioactive compounds were identified in KMLE by liquid chromatography-tandem mass spectrometry (LC-MS/MS). In conclusion, KMLE ameliorated intestinal barrier dysfunction in vitro and in vivo. These findings underscore the potential of KMLE as a therapeutic agent for UC, providing insights into the mechanisms through anti-inflammatory properties and its ability to restore TJ integrity.

Edible and medicinal mushroom polysaccharides (EMMPs) have been widely studied for their various biological activities. It has been shown that EMMPs could modulate microbiota in the large intestine and improve intestinal health. However, the role of EMMPs in protecting the gastric barrier, regulating gastric microbiota, and improving gastric health cannot be ignored. Hence, this review will elucidate the effect of EMMPs on gastric and intestinal barriers, with emphasis on the interaction of EMMPs with microbiota in maintaining overall gastrointestinal health. Additionally, this review highlights the gastroprotective effects and underlying mechanisms of EMMPs against gastric mucosa injury, gastritis, gastric ulcer, and gastric cancer. Furthermore, the effects of EMMPs on intestinal diseases, including inflammatory bowel disease, colorectal cancer, and intestinal infection, are also summarized. This review will also discuss the future perspective and challenges in the use of EMMPs as a dietary supplement or a nutraceutical in preventing and treating gastrointestinal diseases.

Hypoxia-inducible factor (HIF)-1 is a transcription factor that regulates the expression of target genes associated with oxygen homeostasis under hypoxic conditions, thereby contributing to tumor development and progression. Accumulating evidence has demonstrated that HIF-1α mediates different biological processes, including tumor angiogenesis, metastasis, metabolism, and immune evasion. Thus, overexpression of HIF-1α is strongly associated with poor prognosis in cancer patients. Natural compounds are important sources of anticancer drugs and studies have emphasized the decisive role of these mediators in modulating HIF-1α. Therefore, the pharmacological targeting of HIF-1α has emerged as a novel cancer therapeutic approach in recent years. The novelty of this review is that it summarizes natural products targeting HIF-1α in colorectal cancer that have not been presented earlier. We studied research publications related to the HIF-1α domain in cancer from 2010 to 2024. However, our main focus was to identify a better targeted approach for colorectal carcinoma management. Our review described HIF-1α role in tumor progression, summarizes the natural compounds employed as HIF-1α inhibitors, and discusses their potential in the development of natural compounds as HIF-1α inhibitors for colorectal cancer treatment.

Background: Glutamine peptides refer to a series of peptides containing glutamine, and the activity of glutamine peptides is characterized by the content of non-nitrogen terminal glutamine in the peptide. It has been found that glutamine peptides are a stable substitute for glutamine monomer, and they are increasingly studied in nutrition and physiology due to their functional properties. Methods: An extensive search of the literature was conducted in the PubMed, Web of Science, Scopus, and Google Scholar databases up to December 2024. Inclusion criteria focused on the role of glutamine peptides in intestinal health, and the included literature was screened and summarized. Results: This study systematically reviews the current status of research on the preparation, analysis, applications of glutamine peptides and their role in intestinal barrier protection. Furthermore, the challenges faced by the current research and the development direction in the future are discussed. Conclusions: Glutamine peptides can play a role in protecting the intestinal barrier by regulating tight junctions, mucin, inflammatory response, and intestinal flora. In addition, further and intensive investigations are urgently required to address the current challenges pertaining to the structure-activity relationships of glutamine peptides and their transport and absorption mechanism in the gut. This review contributes to a better understanding of the mechanism of glutamine peptides to protect intestinal barrier function and also provides a reference for the development of functional foods with protective effects of intestinal barrier function.

Food allergy has become a global food safety issue, and inducing tolerance of the immune system to allergens is seen as an effective way to address this problem. In this study, shrimp (Penaeus vannamei) was covalently modified with fucoidan to explore its potential as an oral tolerance inducer. The results showed that this strategy not only had no adverse effect on the growth of mice but also achieved significant immune tolerance induction effects. Specifically, it significantly reduced specific antibody levels, improved vascular permeability and intestinal barrier function, and inhibited mast cell degranulation. Further studies showed that these positive results were related to tolerogenic peptides (SLLKANIQL, GLTEFQAV, GDFPGAFKVF, ALNLNPTLALI, and AALDIDSKPF) produced in shrimp allergens. Moreover, this strategy mainly down-regulated gene expression in exogenous substance metabolic and immune-related signaling pathways, thereby reducing immune response to antigens. Overall, fucoidan-mediated covalent modification promises to be an efficient method for producing oral tolerance inducers.

Acute hepatic injury is a severe condition that is always accompanied by oxidative stress and inflammation, seriously threatening the health of the host. Probiotics have been shown to be involved in the regulation of antioxidant system and gut microbiota activity, but studies on the effects of yak derived Bacillus subtilis (B. subtilis) on acute liver injury and oxidative stress remain scarce. Here, we aim to explore the ameliorative effects of B. subtilis isolated from yaks on oxidative stress and hepatic injury caused by D-galactose, as well as the underlying processes. Results indicated that B. subtilis administration, particularly the BS3, significantly mitigated hepatic damage induced by D-galactose in mice as evidenced by ameliorating liver tissue damage as well as decreasing ALT (p < 0.05) and AST (p < 0.05) levels. Additionally, the B. subtilis intervention was demonstrated to enhance the antioxidant system in D-galactose-exposed mice, as manifested by increased T-AOC and SOD, alongside a decrease in MDA levels (p < 0.05). Meanwhile, B. subtilis intervention could effectively mitigate oxidative damage via modulating the Keap1/Nrf2 signaling pathway. Importantly, B. subtilis exhibited a pronounced protective effect against D-galactose-induced intestinal barrier dysfunction through improving tight junction proteins. The gut microbiota results suggest that BS3 alters the abundance of some gut flora such as Firmicutes phylum and Oscillibacter and Lachnospiraceae_NK4A136 genera, which affects the composition of the gut microbiota and reverses the decrease in the microbial richness index in mice. In summary, these findings demonstrated that B. subtilis isolated from yaks serve as a promising candidate to ameliorate oxidative damage and hepatic injury. Meanwhile, the positive regulation effect of B. subtilis on gut microbiota and intestinal mucosal barrier may be one of its underlying mechanisms to alleviate oxidative stress and hepatic injury.

A 12-week aquaculture trial was conducted to evaluate the effects of vitamin B6 on the intestinal health of largemouth bass (Micropterus salmoides). Six feeds with a vitamin B6 content of 2.03 (control group), 2.91, 3.30, 6.03, 9.53, and 21.79 mg/kg were prepared. The results were as follows. Regarding digestive efficiency, the 9.53 mg/kg group showed significantly higher activities of AMY, LPS, and TRY compared to the control group; the 6.03 mg/kg group exhibited increased AKP and Na+/K+ ATPase activities. Regarding immunity, the 6.03 mg/kg group had markedly higher relative expressions of zo-1 and occ than the control group; the 9.53 mg/kg group showed significantly higher relative expressions of il-10, tgf-β, igm, and cd83, while il-8 and tnf-α were notably lower, and nf-κb was noticeably decreased in 21.79 mg/kg group. For antioxidant capacity, the 6.03 mg/kg group had markedly higher activities of CAT, SOD, GSH-Px, and T-AOC levels, compared to the control group; the MDA level in the control group was markedly higher than in the other groups. The relative expressions of nrf2, cat, Cu-Zn sod, and gpx were highest in 9.53 mg/kg group and significantly higher than in the control group. In conclusion, an appropriate level of vitamin B6 in the feed is vital for protecting the intestinal health of largemouth bass.

Mare milk (MM) and fermented mare milk (FM) are specialized animal milks with high nutritional value, containing a variety of functionally active substances that are capable of resisting inflammatory responses and oxidative stress. However, little relevant research on the maintenance of intestinal homeostasis has been performed. This study aimed to investigate the effects of MM and FM on the prevention of dextran sulfate sodium salt (DSS)-induced ulcerative colitis in a mouse model and to preliminarily elucidate the underlying mechanisms. The results showed that MM and FM had different degrees of protective effects against the damage caused by DSS and alleviated ulcerative colitis by inhibiting weight loss, reducing colon length shortening, and restoring intestinal structure. Additionally, MM and FM maintained intestinal tight junction protein levels to repair barrier function, downregulated inflammatory cytokines (e.g., IL-1β, TNF-α, IL-6, and iNOS) and bolstered the body's antioxidant defense system. Moreover, MM and FM regulated dysregulation of the intestinal microenvironment by improving the diversity of the gut microbiota and reshaping its structure, including increasing the proportion of Firmicutes and Bacteroidetes and the relative abundance of beneficial bacterial genera (e.g., Akkermansia). In summary, MM and FMM can serve as dietary resources for preventing ulcerative colitis and maintaining intestinal homeostasis.

Osteoarthritis (OA) is a chronic, progressive degenerative joint disease that affects the entire synovial joint, leading to the progressive degeneration of articular cartilage. It seriously affects the quality of life and global disability of patients. OA is affected by a variety of factors; the most significant risk factor for OA is age. As individuals age, the risk and severity of OA increase due to the exacerbation of cartilage degeneration and wear and tear. In recent years, research has indicated that the gut microbiota may play a significant role in the aging and OA processes. It is anticipated that regulating the gut microbiota may offer novel approaches to the treatment of OA. The objective of this paper is to examine the relationship between the gut microbiota and senile OA, to investigate the potential mechanisms involved. This review also summarizes the therapeutic strategies related to gut flora in OA management, such as prebiotics and probiotics, diet, exercise, traditional Chinese medicine (TCM) modification, and fecal microbiota transplantation (FMT), highlighting the potential clinical value of gut flora and elucidating the current challenges. The foundation for future research directions is established through the summarization of current research progress.

Probiotics effectively alleviate host diarrhoea, but the specific mechanism is not clear. Therefore, we explored the protective mechanism of Bacillus coagulans (BC) on intestinal barrier injury induced by Klebsiella pneumoniae (K. pneumoniae) in rabbits by HE, immunofluorescence and 16S rRNA. The results showed that BC pretreatment alleviated the changes in average daily gain, average daily feed intake and FCR caused by K. pneumoniae in rabbits. Moreover, BC alleviated the inflammatory cell infiltration, intestinal villus reduction, crypt deepening and goblet cell reduction caused by K. pneumoniae in rabbits. Further research revealed that BC improved the intestinal barrier by improving the mechanical barrier, chemical barrier, immune barrier and microbial barrier. Specifically, BC improved the intestinal mechanical barrier by improving the intestinal structure, increasing the protein expression of PCNA, increasing the number of goblet cells, and altering the expression of occludin, claudin-1 and ZO-1. BC improved the intestinal chemical barrier by regulating the expression of MUC1 and MUC2 and inhibited the TLR4/MyD88/NF-κB signalling pathway by altering the expression levels of the inflammatory factors IL-1β, IL-6 and TNF-α, thus optimizing the intestinal immune barrier. In addition, adding BC to the diet improved the intestinal microbial barrier of rabbits by reducing the abundance of harmful bacteria and increasing the abundance of beneficial bacteria. In summary, BC protects against K. pneumoniae-induced intestinal barrier damage by improving intestinal morphology, mitigating the inflammatory response and regulating the microbial composition. Among the pretreatments, the pretreatment effect of 1 × 106 CFU/g was the best. This study provides a theoretical basis for the use of BC to prevent and treat diarrhoea caused by K. pneumoniae in rabbits.

Persistent organic pollutants (POPs) are pervasive organic chemicals with significant environmental and ecological ramifications, extending to adverse human health effects due to their toxicity and persistence. The intestinal mucosal barrier, a sophisticated defense mechanism comprising the epithelial layer, mucosal chemistry, and cellular immunity, shields the host from external threats and fosters a symbiotic relationship with intestinal bacteria. Sirtuin 6 (SIRT6), a sirtuin family member, is pivotal in genome and telomere stability, inflammation regulation, and metabolic processes. Result shows POPs have been implicated in the intestinal diseases, particularly in intestinal barrier dysfunction, through mechanisms such as cellular damage, epigenetic alterations, inflammation, microbiota changes, and metabolic disruptions. While the impact of SIRT6 expression changes on intestinal barrier functions has been reviewed, the mechanisms linking POPs to SIRT6 remain elusive. This review summarized the latest research results on the effects of POPs on intestinal barrier, discussed the role of SIRT6 from multiple mechanism perspectives, proposed new research directions on POPs, SIRT6 and intestinal health, and explored the therapeutic potential of SIRT6.

We have examined some effects of administering vitamin D and extract of common nettle (Urtica dioica) to rats with experimentally induced Crohn's disease (CR). Body weight and colon length were lower in the CR group than in normal controls, whereas scores for histopathologic changes seen in sections stained by the H&E and PAS methods were lower in rats with CR than in those that also received either vitamin D (CRD) or nettle extract (CRI). Strong manganese-superoxide dismutase (Mn-SOD) immunoreactivity was detected in the crypt epithelium of the CR and CRI groups and in the lymphoid tissue of the CRD group. Weak catalase (CAT) immunoreactivity in the crypt epithelium in the CR, CRI, and CRD groups and strong CAT immunoreactivity in the lymphoid tissue in the CR group were also observed. Our results reveal that administering either vitamin D and common nettle extract can have augment Mn-SOD and CAT expression in colon tissues and contribute to alleviation of some complications of experimental Crohn's disease.

The aim of this study is to examine the physiological effects of emodin on intestinal microorganisms and the liver in the BALb/c mice.

Following an 8-week administration of emodin at doses of 25, 50, and 100 mg/kg/day,pathological analyses revealed that emodin significantly reduced the colon length, induced colonic crypt inflammation,diminished the colonic mucus layer,and decreased the fluorescence intensity of colonic tight junction proteins ZO-1 and Occludin. Concurrently, 16S rDNA gene sequencing corroborated that emodin altered the diversity and composition of the intestinal microbiota by increasing the Firmicutes to Bacteroides ratio. Simultaneously, the non-targeted metabolomics analyses exhibited significant alternations in both short chain fatty acids and free fatty acids between the emodin-treated and the normal groups, indicating emodin-induced disturbance in intestinal metabolic disorder. Furthermore, emodin exhibited a significant elevation in LPS levels in colon, serum and liver as well an marked increase in the levels of TC, TG, AST, and ALT in serum. Additionally, histological examination employing by HE and oil-red O staining furtherly verified that the administration of varying doses emodin induced hepatic inflammation and lipid accumulation. Whereas qRT-PCR and Western blot analyses demonstrated that the administering of varying doses of emodin upregulated the mRNA levels of TNF-α, IL-1β, IL-6, and IL-18 as well as the expression of TLR4, Myd88, and P-65. Following the combined administration of probiotics, the high-dose emodin did not significantly influence ALT and AST levels in mice. However, the faeces of the high-dose emodin transplanted in mice and induced a significant increase in AST levels and in the relative abundance of Firmicutes and Proteobacteria.

These findings further corroborate that emodin induces liver injury via the intestinal dysfunction. These findings suggested that emodin may disrupt intestinal microbiota and resulted in significant alternations in endogenous metabolites in mice, thereby facilitating the entry of LPS and FFAs into the liver, potentially leading to hepatic injury.

Mycotoxins are ubiquitous natural pollutants that pose a serious threat to public health. Deoxynivalenol (DON) as one of the most prominent mycotoxins has a noticeable adverse effect on intestinal barrier function, which depends on the intestinal barrier integrity. However, the potential mechanisms and effective therapeutic strategies remain unclear. Aryl hydrocarbon receptor (AHR) has been implicated in the modulation of intestinal barrier function and inflammation. The study aims to investigate the unique role of AHR in mediating DON-induced intestinal epithelial barrier function. In the current study, we revealed that DON triggered mitochondrial structural damage and functional impairment, leading to oxidative stress and apoptosis in porcine jejunal epithelial cells (IPEC-J2). DON altered the integrity of IPEC-J2 cells by disrupting the distribution and function of tight junction proteins. Additionally, DON activated TNF-α/NF-κB/MLCK signaling pathway, thereby eliciting inflammatory response. Notably, DON inhibited AHR nuclear translocation and attenuated xenobiotic response element promoter activity and its target genes. However, overexpression of AHR mitigated DON-induced disruption of intestinal epithelial barrier functions by suppressing TNF-α/NF-κB/MLCK pathway in IPEC-J2 cells. Our findings indicate that AHR regulates intestinal epithelial barrier function and therefore is a novel therapeutic molecule for intestinal disorders.

Ulcerative colitis (UC) is a complex, refractory inflammatory bowel disease characterized impared intestinal mucosal barrier and imbalanced M1/M2 macrophage polarization mediating its progression. Formononetin (FN), a bioactive isoflavone with established anti-inflammatory and immunomodulatory properties, shows promise in mitigating UC, yet its therapeutic and underlying mechanisms remain unclear. In this study, colitis was induced in mice by administering 2.5% (w/v) dextran sulfate sodium (DSS) solution for 7 days. Oral (25, 50, and 100 mg/kg) FN for 10 days significantly ameliorated colitis symptoms in a dose-dependent manner, by mitigating body weight loss, reducing disease activity index (DAI), colonic weight, and colonic weight index, while enhancing survival rates and colonic length. Histological analysis revealed FN remarkably suppressed inflammatory damage in colonic tissues. Furthermore, FN modulated the expression of pro- and anti-inflammatory cytokines and enhanced antioxidant capacity. Notably, FN treatment significantly enhanced the expression of tight junction (TJ) proteins (claudin-1, ZO-1, occludin) at both protein and mRNA levels in the colon tissues, suggesting improved intestinal barrier function. Crucially, FN inhibited macrophage infiltration in colonic tissues and rebalanced M1/M2 macrophage polarization. While, macrophage depletion largely abrogated FN's protective effects against colitis, indicating a crucial role for macrophages in mediating FN's therapeutic response. Overall, FN effectively alleviated colitis primarily via modulating inflammatory cytokine expression, enhancing antioxidant capacity, upregulating TJs proteins expression, and remodeling M1/M2 macrophage polarization equilibrium. These findings suggest that FN could be the next candidate to unlocking UC's treatment challenge.

Floccularia luteovirens polysaccharides (FLP1s) have potential biological activities. Our previous study showed that FLP1s positively regulated gut immunity and microbiota. However, it is still unclear whether FLP1s mediate gut microbiota in immunosuppressed mice. This research aims to explore the relationship between FLP1-mediated gut microbes and intestinal immunity in immunosuppressed mice through fecal microbiota transplantation (FMT). The results demonstrated that FLP1s exhibited prebiotic and anti-immunosuppressive effects on CTX-induced immunosuppressed mice. FFLP1 treatment (microbiota transplantation from the fecal sample) remarkably elevated the production of sIgA and secretion of the anti-inflammatory cytokines IL-4, TNF-α, and IFN-γ in the intestine of CTX-treated mice, inducing activation of the MAPK pathway. Moreover, FFLP1s mitigated oxidative stress by activating the Nrf2/Keap1 signaling pathway and strengthened the intestinal barrier function by upregulating the expression level of tight junction proteins (occludin, claudin-1, MUC-2, and ZO-1). Furthermore, FFPL1s restored gut dysbiosis in CTX-treated immunosuppressed mice by increasing the abundance of Alloprevotella, Lachnospiraceae, and Bacteroides. They also modified the composition of fecal metabolites, leading to enhanced regulation of lipolysis in adipocytes, the cGMP-PKG pathway, the Rap1 signaling pathway, and ovarian steroidogenesis, as indicated by KEGG pathway analysis. These findings indicate that FLP1s could modulate the response of the intestinal immune system through regulation of the gut microbiota, thus promoting immune activation in CTX-treated immunosuppressed mice. FLP1s can serve as a natural protective agent against CTX-induced immune injury.

Intestinal fibrosis, a common complication of inflammatory bowel disease, in particular in Crohn's disease, arises from chronic inflammation, leading to intestinal narrowing, structural damage, and functional impairment that significantly impact patients' quality of life. Current treatment options for intestinal fibrosis are limited, with surgery being the primary intervention. Traditional Chinese Medicine (TCM) has emerged as a promising approach in preventing and treating intestinal fibrosis. However, there is a scarcity of literature summarizing the mechanisms underlying TCM's efficacy in this context. To address this gap, we conducted a comprehensive review, uncovering multiple mechanisms through which TCM mitigates intestinal fibrosis. These mechanisms include immune cell balance regulation, suppression of inflammatory responses, reduction of inflammatory mediators, alleviation of colon tissue damage, restoration of intestinal function, modulation of growth factors to inhibit fibroblast activation, dynamic regulation of TIMPs and MMPs to reduce extracellular matrix deposition, inhibition of epithelial-mesenchymal transition and endothelial-mesenchymal transition, autophagy modulation, maintenance of the intestinal mucosal barrier, prevention of tissue damage by harmful factors, and regulation of cell proliferation and apoptosis. This study aims to bridge existing knowledge gaps by presenting recent evidence supporting the utilization of TCM in both clinical and experimental research settings.

The transient receptor potential vanilloid 4 channel (TRPV4) is an important member of the TRP superfamily of cation channels. The channel can be activated by different physical and chemical stimuli, such as heat, osmotic, and mechanical stress. It regulates the release of nociceptive peptides (substance P and calcitonin gene-related peptide), and mediates neurogenic inflammation, which indicates the involvement of TRPV4 as a nociceptor. Previous studies show that TRPV4 regulates the contraction of intestinal smooth muscle, mucosal barrier permeability, intestinal ion transport, activation of submucosal enteric neurons, and generation of immune cells. TRPV4 is involved in various pathophysiological activities, and altered TRPV4 expression has been detected in some intestinal diseases (IBD, IBS, intestinal tumors, etc). Evidence indicates that TRPV4 plays a noxious role in intestinal barrier function when the intestine is damaged. This review focuses on the role of the TRPV4 channel in the physiological and pathological functions of the intestine, and evaluates the potential clinical significance to target TRPV4 channel in the treatment of intestinal diseases.

Inflammatory bowel disease (IBD) is a chronic immune-inflammatory disease. Gut microbes, intestinal immunity, and gut barrier function play a critical role in IBD. Growing evidence suggests that synbiotic may offer therapeutic benefits for individuals with colitis, suggesting an alternative therapy against colitis. With this in mind, we creatively prepared a new synbiotic combination consisting of a probiotic strain (Limosilactobacillus reuteri) along with one prebiotic chitooligosaccharides (COS). The protective effects of the synbiotic on DSS-induced colitis and the underlying mechanisms were investigated. We demonstrated that the synbiotic ameliorated colitis in mice, as evidenced by a significant remission in body weight loss and colon shortening, and a decreased disease activity index (DAI). Notably, synbiotic reduced the intestinal inflammation and injury by synergistically decreasing inflammatory factors, inhibiting TLR4/Myd88/NF-κB/NLRP3 signaling, preventing macrophage infiltration, and enhancing the integrity of the intestinal barrier. Moreover, synbiotic selectively promoted the growth of beneficial bacteria (e.g., Akkermansia, Lactobacillus) but decreased the pathogenic bacteria (e.g., Helicobacter). BugBase's analysis supported its ameliorated role in reducing pathogenic bacteria. Collectively, our findings revealed the novel synbiotic had a potential to treat colitis, which was associated with its anti-inflammatory and microbiota-balancing properties. This study will contribute to the development of functional synbiotic products for IBD therapy and will provide valuable insights into their mechanisms.

This study was conducted to explore the protective effects of inulin against lipopolysaccharide (LPS)-induced inflammatory response and intestinal barrier dysfunction in broilers. 108 broilers were allocated to 3 treatments: 1) non-challenged broilers (Control, CON); 2) LPS-challenged broilers (LPS); 3) LPS-challenged broilers fed the basal diet supplemented with 15 g/kg of inulin (Inulin + LPS). At 21 d of age, the LPS-challenged groups received an intraperitoneal injection of LPS, and the CON group received an equal volume of saline. After 4 h of LPS exposure, samples of blood, intestinal mucosa and cecal digesta were collected. The results showed that LPS challenge induced systemic inflammation and damaged intestinal barrier function, whereas inulin attenuated LPS-induced production of pro-inflammatory cytokines by inhibiting the activation of TLR4 and NF-κB p65, and enhanced intestinal barrier function. In addition, LPS stimulation caused cecal microbial dysbiosis as shown by increased abundance of pathogenic bacteria including Ruminococcus_torques_group, Escherichia-Shigella and Subdoligranulum, while supplementation of inulin increased abundance of beneficial bacteria Faecalibacterium and Anaeroplasma, and metabolite production including propionate and butyrate concentrations. In conclusion, dietary supplementation of inulin could partially alleviate LPS-induced inflammation and intestinal barrier injury by modulating intestinal microbiota, thereby minimizing growth retardation of broilers. Our results provide a basis for the rational utilization of inulin in alleviating immune stress in broiler production.

Colostrum is the initial secretion of the mammary glands following parturition, which offers main food, protection, and biological active substances for the new born. The most threatening episode of neonate's life is the initial two weeks after birth. This period is associated with high neonatal mortality and morbidity. These worthwhile losses lead to a poor prolificacy rate, low profitability, and ultimately poor performance in animal production. Hence, both diseases and mortality cause valuable losses in terms of production and economic losses. The survival of neonate is correlated with their immune status and passive immune transfer (PIT). Colostrum provides the primary source of nutrition and immunity (PIT) that protects neonates against infections. It must be given as soon as possible after birth since its immunoglobulins are absorbed within the first 16-27 hours after birth, ideally within 2-4 hours. As a result, immunoglobulin (PIT) is the most important component of distressing infectious immunity, and a passable concentration of immunoglobulin in the blood of newborn lambs is linked to their health and survival rate. In this review, we summarized the importance of colostrum in early life and its association with neonatal lamb's survival, profitability and productivity of sheep farming.

Microcystin-LR (MC-LR) and nitrites from the environment and daily life can be ingested and absorbed by humans via the digestive tract. However, their combined effects on intestinal health remain unclear. Here, the combined impact of MC-LR and sodium nitrite (NaNO2) on the intestines of mice was investigated under actual human exposure conditions. After mice were exposed to MC-LR (10, 100 μg/L) and NaNO2 (30, 300 mg/L) individual and in combination for 6 months, it was found that MC-LR and NaNO2 synergistically decreased intestinal permeability and disrupted intestinal physical, chemical, immune, and microbial barriers. In the coexposure groups, the synergistic impairment to the intestinal barrier was noted with increasing concentrations of MC-LR or NaNO2, but this adverse effect was alleviated by nicotinamide supplementation. This study underscores the potential risks of simultaneous ingestion of MC-LR and nitrite on intestinal health. The protective role of nicotinamide suggests avenues for therapeutic intervention against environmental toxin-induced intestinal impairment.

Acute lung injury (ALI) is associated with high morbidity and mortality rates. However, its clinical treatment is limited. Currently, the treatment of lung diseases by regulating the lung microbiota has become a research hotspot. In this study, we investigated the protective effects of the intranasal administration of Clostridium butyricum and its derived extracellular vesicles (EVs) against lipopolysaccharide (LPS)-induced ALI. The results demonstrated that compared with the LPS group, the pre-treatment group with C. butyricum and its EVs reduced the expression of pro-inflammatory cytokines and alleviated the symptoms in ALI mice by inhibiting the TLR4/MyD88 signaling pathway. Moreover, C. butyricum and its derived EVs inhibited the expression of apoptosis-related proteins and increased the expression of lung barrier proteins. Additionally, the intervention of C. butyricum changed the composition of the pulmonary microbiota. At the species level, LPS significantly increased the relative abundance of Acinetobacter johnsonii, while C. butyricum reversed this effect. In conclusion, these data demonstrate that intranasal administration of C. butyricum and its EVs can prevent LPS-induced ALI by reducing inflammation, inhibiting apoptosis, and improving lung barrier function. Additionally, C. butyricum regulated the pulmonary microbiota of mice to alleviate LPS-induced ALI.IMPORTANCEThe disorder of pulmonary microbiota plays an important role in the progression of acute lung injury (ALI). However, very few studies have been conducted to treat ALI by modulating pulmonary microbiota. In this study, the diversity and composition of pulmonary microbiota were altered in lipopolysaccharide (LPS)-induced ALI mice, but the ecological balance of the pulmonary microbiota was restored by intranasal administration of Clostridium butyricum. Moreover, the study reported the mechanism of C. butyricum and its derived extracellular vesicles for the treatment of LPS-induced ALI. These results reveal the importance of pulmonary microbiota in ALI disease. It provides a new approach for the treatment of ALI with new-generation probiotics.

Exosomes derived from endometrial regenerative cells (ERC-Exos) can inherit the immunomodulatory function from ERCs, however, whether ERC-Exos exhibit such effect on inflammatory bowel diseases with mucosal immune dysregulation has not been explored. Insulin-like growth factor-Ⅱ (IGF2) is considered to possess the potential to induce an anti-inflammatory phenotype in immune cells. In this study, the contribution of IGF2 in mediating the protective efficacy of ERC-Exos on colitis was investigated.

Lentiviral transfection was employed to obtain IGF2-specific knockout ERC-Exos (IGF2-/--ERC-Exos). Experimental colitis mice induced by dextran sulfate sodium (DSS) were divided into the phosphate-buffered saline (untreated), ERC-Exos-treated and IGF2-/--ERC-Exos-treated groups. Colonic histopathological analysis and intestinal barrier function were explored. The infiltration of CD4+ T cells and dendritic cells (DCs) were analyzed by immunofluorescence staining and flow cytometry. The maturation and function of bone marrow-derived dendritic cells (BMDCs) in different exosome administrations were evaluated by flow cytometry, ELISA and the coculture system, respectively.

Compared with the untreated group, ERC-Exos treatment significantly attenuated DSS-induced weight loss, bloody stools, shortened colon length, pathological damage, as well as repaired the weakened intestinal mucosal barrier, including promoting the goblet cells retention, restoring the intestinal barrier integrity and enhancing the expression of tight junction proteins, while the protective effect of exosomes was impaired with the knockout of IGF2 in ERC-Exos. Additionally, IGF2-expressing ERC-Exos decreased the proportions of Th1 and Th17, increased the proportions of Treg, as well as attenuated DC infiltration and maturation in mesenteric lymph nodes and lamina propria of the colitis mice. ERC-Exos were also observed to be phagocytosed by BMDCs and IGF2 is responsible for the modulating effect of ERC-Exos on BMDCs in vitro.

Exosomes derived from ERCs can exert a therapeutic effect on experimental colitis with remarkable alleviation of the intestinal barrier damage and the abnormal mucosal immune responses. We emphasized that IGF2 plays a critical role for ERC-Exos mediated immunomodulatory function and protection against colitis.

The intestinal mucosal barrier (IMB) damage is intricately linked with the onset of numerous intestinal diseases. Astragalin (AS), a flavonoid present in numerous edible plants, exhibits notable antioxidant and anti-inflammatory properties, demonstrating a promising impact on certain intestinal ailments. In this study, our objective was to investigate the protective effects of AS and elucidate the underlying mechanisms by which it mitigates lipopolysaccharide (LPS)-induced damage to the IMB in mice.

During the experimental period, mice were subjected to a 7-day regimen of AS treatment, followed by LPS injection to induce IMB damage. Subsequently, a comprehensive evaluation of relevant biological indicators was conducted, including intestinal pathological analysis, serum inflammatory factors, intestinal tight junction proteins, and intestinal microbiota composition.

Our results suggested that AS treatment significantly bolstered IMB function. This was evidenced by the enhanced morphology of the small intestine and the elevated expression of tight junction proteins, including ZO-1 and Claudin-1, in addition to increased levels of MUC2 mucin. Moreover, the administration of AS demonstrated a mitigating effect on intestinal inflammation, as indicated by the reduced plasma concentrations of pro-inflammatory cytokines such as IL-6, IL-1β, and TNF-α. Furthermore, AS treatment exerted a positive influence on the composition of the gut microbiota, primarily by augmenting the relative abundance of beneficial bacteria (including Lachnospiracea and Lactobacillus murinus), while simultaneously reducing the prevalence of the harmful bacterium Mucispirillum schaedleri.

AS mitigates LPS-induced IMB damage via mitigating inflammation and modulating intestinal microbiota.

Being the first line of defense, intestinal mucosal immunity serves as in maintaining immune homeostasis among organisms. This study investigated the impact of the areca inflorescence polysaccharide (AFP) on intestinal mucosal immunity and elucidated the mechanisms responsible for the immunomodulatory effects of AFP. The immunosuppression mouse model was established using the cyclophosphamide. The intestinal mucosal status was evaluated based on the intestinal integrity, chemical and mucosal immune barriers, and intestinal flora. According to the findings, AFP enhances intestinal integrity by up-regulating the expression of tight junction proteins and reinforcing the chemical barrier through increased mucin-2, β-defensins, and SIgA expression and secretion. Furthermore, AFP restores the mucosal immune barrier by regulating immune cells within Peyer's patches and lamina propria. AFP also reverses the intestinal flora balance and regulates its metabolism. Additionally, AFP effectively modulates the immune response in the spleen and peripheral blood. Together, these results indicated that AFP repairs mucosal damage and restores mucosal immunity, thereby preserving the immune homeostasis of organisms.

The microbiome plays a crucial role in integrating environmental influences into host physiology, potentially linking it to autoimmune liver diseases, such as autoimmune hepatitis, primary biliary cholangitis, and primary sclerosing cholangitis. All autoimmune liver diseases are associated with reduced diversity of the gut microbiome and altered abundance of certain bacteria. However, the relationship between the microbiome and liver diseases is bidirectional and varies over the course of the disease. This makes it challenging to dissect whether such changes in the microbiome are initiating or driving factors in autoimmune liver diseases, secondary consequences of disease and/or pharmacological intervention, or alterations that modify the clinical course that patients experience. Potential mechanisms include the presence of pathobionts, disease-modifying microbial metabolites, and more nonspecific reduced gut barrier function, and it is highly likely that the effect of these change during the progression of the disease. Recurrent disease after liver transplantation is a major clinical challenge and a common denominator in these conditions, which could also represent a window to disease mechanisms of the gut-liver axis. Herein, we propose future research priorities, which should involve clinical trials, extensive molecular phenotyping at high resolution, and experimental studies in model systems. Overall, autoimmune liver diseases are characterized by an altered microbiome, and interventions targeting these changes hold promise for improving clinical care based on the emerging field of microbiota medicine.

A recent review proposed a role for multi-functional food or supplement products in priming the gut to support both digestive and systemic health. Accordingly, we designed and eva-luated the effect of a multi-functional gastrointestinal (GI) primer supplement on participant-reported measures for digestive health, quality-of-life (e.g., energy/vitality and general health), and reasons for satiation (e.g., attitudes towards food and eating). In this single-arm clinical trial, 68 participants with mild digestive symptoms consumed the GI primer supplement daily for 14 days. Digestive symptoms were evaluated daily from baseline (Day 0) through Day 14. At baseline and Day 14, participants reported their stool consistency, reasons for satiation, and quality-of-life measures using validated questionnaires. At Day 14, participants reported significant improvements in all (13/13) digestive symptom parameters (p-values < 0.05) and an increase in % of stools with normal consistencies. There were significant improvements (p-values < 0.05) in energy/vitality and general health, and in specific attitudes towards food and eating (e.g., physical satisfaction, planned amount, decreased eating priority, decreased food appeal, and self-consciousness). Results suggest the GI primer supplement promotes digestive health, improves quality of life, and impacts attitudes towards food/eating. This study provides preliminary support for the gut priming hypothesis through which multi-functional digestive products may improve GI health.

Trace minerals are essential for biological processes, including enzyme function, immune response, and hormone synthesis. The study assessed the effects of different dietary trace minerals on the gut health, microbiota composition, and immune function of cats. Eighteen adult British Shorthair cats were divided into three groups receiving inorganic trace minerals (ITM), a 50/50 mix of inorganic and organic trace minerals (ITM + OTM), or organic trace minerals (OTM) for 28 days. The OTM showed enhanced immune capacities, reduced intestinal barrier function, and lower inflammation condition. The OTM altered gut microbiota diversity, with a lower Simpson index and higher Shannon index (p < 0.05). Specifically, the abundance of Bacteroidota, Lachnospiraceae, and Prevotella in the OTM group were higher than the ITM group (p < 0.05). Metabolomic analysis identified 504 differential metabolites between the OTM and ITM groups (p < 0.05, VIP-pred-OPLS-DA > 1), affecting pathways related to steroid hormone biosynthesis and glycerophospholipid metabolism (p < 0.05, VIP-pred-OPLS-DA > 2). Additionally, there was a significant correlation between intestinal microbiota and differential metabolites. To conclude, dietary OTM can modulate the gut metabolite and microbiota composition, enhance immune and intestinal barrier function, and mitigate inflammation in cats, highlighting the benefit of using OTM in feline diet to promote the intestinal and overall health.

Intestinal barrier dysfunction is a significant contributor to the recurrence and refractory of ulcerative colitis (UC). Promoting the interaction between group 3 innate lymphoid cells (ILC3s) and gut flora is a valuable strategy for mucosal repair. Paeoniae decoction (PD) is a compound commonly used in clinical treatment of UC, but its exact mechanism remains unclear.

We aimed to investigate the protective effect of PD on intestinal mucosal injury induced by dextran sulfate sodium (DSS) in chronic colitis, as well as to elucidate its potential mechanism.

C57BL/6 mice were induced with chronic colitis by 2 % DSS and divided into four groups: control group, model group, PD low dose (4 g/kg), and high dose (8 g/kg) group. The effectiveness of PD in treating chronic colitis mice was evaluated based on changes in body weight, colon length, colon pathological tissue scores, and the mRNA levels of inflammatory factors IL-6 and IL-1β. The expressions of intestinal epithelial tight junction proteins (ZO-1 and Occludin), IL-22, and MUC2 were observed using immunofluorescence and RT-PCR. Additionally, the proportion of ILC3 and natural cytotoxicity receptor (NCR)+ ILC3 in the colon were detected using flow cytometry. Furthermore, UHPLC-QE-MS was utilized to identify chemical components of PD and network pharmacology was employed to predict potential pathways for PD intervention in UC. Subsequently, MNK-3 cells (ILC3 in vitro cell line) and NCM460 cells were used to verify the network pharmacology results. Finally, the effects of PD on UC gut flora have been explored using in vitro fermentation and 16S rDNA techniques.

The results showed that PD significantly restored body weight and colon length in mice with chronic colitis, while also reducing colon inflammatory cell infiltration and the expression of IL-6 and IL-1β. Additionally, PD notably promoted the expression of MUC2, ZO-1, Occludin, and IL-22, as well as increasing the ratio of ILC3 and NCR+ILC3. UHPLC-QE-MS analysis identified 443 components of PD, and network pharmacology suggested that PD could target the aryl hydrocarbon receptor (AHR) signaling pathway, which was confirmed by MNK-3 cells and in vitro fermentation experiments. Furthermore, MNK-3-conditioned medium (CM) increased the expression of ZO-1 and Occludin in NCM460 cells. In addition, 16S rDNA results indicated that PD promoted the abundance of Lactobacillales, thus contributing to mucosal damage repair by activating the AHR signal in ILC3s.

In summary, our study demonstrates that PD repairs intestinal mucosal damage in chronic colitis by regulating the interaction of gut flora with ILC3, and the specific mechanism is related to the activation of AHR signaling pathway.

Inflammatory bowel disease (IBD) refers to long-term medical conditions that involve inflammation of the digestive tract, and the global incidence and prevalence of IBD are on the rise. Gut microbes play an important role in maintaining the intestinal health of the host, and the occurrence, development, and therapeutic effects of IBD are closely related to the structural and functional changes of gut microbes. Published studies have shown that the natural products from traditional Chinese medicine have direct or indirect regulatory impacts on the composition and metabolism of the gut microbes. In this review, we summarize the research progress of several groups of natural products, i.e., flavonoids, alkaloids, saponins, polysaccharides, polyphenols, and terpenoids, for the therapeutic activities in relieving IBD symptoms. The role of gut microbes and their intestinal metabolites in managing the IBD is presented, with focusing on the mechanism of action of those natural products. Traditional Chinese medicine alleviated IBD symptoms by regulating gut microbes, providing important theoretical and practical basis for the treatment of variable inflammatory intestinal diseases.