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Impairment of the intestinal epithelium barrier through alteration of proliferation and differentiation balance in alcohol use disorder 认领 引用
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作者 Ami G Toulehohoun Jérôme Ambroise +7 位作者 Bouchra Illiyas Luca Maccioni Joaquim Lupianez Rita Manco Laure-Alix Clerbaux Caroline Bouzin Bernd Schnabl Peter Stärkel 《World Journal of Gastroenterology》 SCIE CAS 2026年第28期112-132,共21页
BACKGROUND Alcohol use disorder(AUD)profoundly affects human health,yet its direct impact on the intestinal epithelium and stem cell niche remains insufficiently understood.AIM To characterize alcohol-induced alterati... BACKGROUND Alcohol use disorder(AUD)profoundly affects human health,yet its direct impact on the intestinal epithelium and stem cell niche remains insufficiently understood.AIM To characterize alcohol-induced alterations in intestinal epithelial morphology,proliferation,differentiation,and barrier-related functions in AUD patients.METHODS Duodenal biopsies from healthy and AUD patients were analyzed for epithelial architecture,proliferation,differentiation activity,and lineage composition using histological,immunofluorescence,proteomic,and transcriptomic approaches.Findings were complemented by studies in human-derived enteroids exposed to 40-or 70-mM ethanol to assess its direct effects on epithelial proliferation and signaling pathways.RESULTS A subset of AUD patients exhibited marked epithelial remodeling,including increased crypt depth,shortened villi,and expanded proliferation in the crypt base and transit-amplifying zone.Ki67+cells and OLFM4+stem-like compartment were increased,with CD44 identified as a potential driver of crypt-base proliferation.Moreover,a higher number of Ki67+crypts co-expressed the enteroendocrine cells marker CHGA+and the stem cell marker OLFM4.Ki67+Kruppel-like factor 4+cells were elevated in transit-amplifying zone,correlating with higher MUC2,MUC5AC,and anterior gradient-2 expression,alongside reduced antimicrobial peptides DEFA5,DEFA6,and REG3A.Nutrient absorption markers MTTP,FABP2,and SLC1A5 were dysregulated.Ethanol-exposed enteroids showed increased Ki67+cells and cyclin B1 mRNA without changes in CD44 or Axin2 indicating a proliferative effect independent of canonical Wnt signaling.CONCLUSION Heavy alcohol consumption induces profound alterations in intestinal epithelial morphology,stem cell niche dynamics,and functional barrier properties.Together,these findings suggest that ethanol disturbs the intestinal proliferation-differentiation balance. 展开更多
关键词 Alcohol use disorder Intestinal epithelium Intestinal barrier Stem cell niche Intestinal organoids Enteroids
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Berberine alleviates experimental colitis by enhancing gutmicrobiota-dependent intestinal barrier function and suppressing gasdermin D activation 认领 引用
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作者 Ping Yang Ran Wang +2 位作者 Yu-Ping Zhou Jin-Feng Wen Dong-Xue Yang 《World Journal of Gastroenterology》 SCIE CAS 2026年第13期97-115,共19页
BACKGROUND Ulcerative colitis(UC)is a chronic,recurrent inflammatory disease of the gastrointestinal tract that often presents challenges in clinical management.Traditional Chinese medicine constitutes a significant t... BACKGROUND Ulcerative colitis(UC)is a chronic,recurrent inflammatory disease of the gastrointestinal tract that often presents challenges in clinical management.Traditional Chinese medicine constitutes a significant therapeutic modality for the management of UC.Berberine has demonstrated remarkable therapeutic potential for the treatment of UC.AIM To determine whether berberine alleviates dextran sulfate sodium(DSS)-induced UC in mice by enhancing gut microbiota-dependent intestinal barrier function and inhibiting gasdermin D(GSDMD)activation.METHODS An acute colitis mouse model was established by administering 3%DSS.The mice were treated daily with berberine(50 mg/kg and 100 mg/kg),after which body weight,colon length,histological scoring,and intestinal levels of inflammatory cytokines were assessed.Intestinal barrier permeability was evaluated,and 16S ribosomal RNA sequencing was conducted.Fecal microbiota transplantation and cohousing studies were performed to determine the role of the gut microbiota.The inhibitory effects of GSDMD were pharmacologically manipulated to substantiate the efficacy and underlying mechanism of action of berberine in treating UC in preclinical models.RESULTS Berberine has shown significant potential for alleviating the severity of DSSinduced acute colitis.Fecal microbiota transplantation and cohousing experiments showed that the gut microbiota is indispensable for the beneficial effects of berberine in DSS-induced colitis.Moreover,pharmacological inhibition of GSDMD attenuated the therapeutic efficacy of berberine,highlighting the importance of GSDMD in the mechanism of action.CONCLUSION Berberine alleviates experimental colitis by inhibiting the GSDMD-mediated pathway and increasing gut barrier function via a microbiota-mediated approach,thus offering a new molecular target for colitis therapy. 展开更多
关键词 Ulcerative colitis Berberine Gasdermin D Intestinal inflammation Intestinal microbiota
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Xpert Ultra and TrueNat MTB plus assays for the diagnosis of gastrointestinal tuberculosis:A diagnostic accuracy study 认领 引用
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作者 Kusum Sharma Neha Jindal +5 位作者 Megha Sharma Harshal S Mandavdhare Pankaj Gupta Aravind Sekar Usha Dutta Vishal Sharma 《World Journal of Gastroenterology》 SCIE CAS 2026年第14期73-80,共8页
BACKGROUND Discriminating between gastrointestinal tuberculosis(GITB)and Crohn’s disease is a perplexing challenge for clinicians.The clinical presentation,endoscopic appearances,radiographic features,and histologica... BACKGROUND Discriminating between gastrointestinal tuberculosis(GITB)and Crohn’s disease is a perplexing challenge for clinicians.The clinical presentation,endoscopic appearances,radiographic features,and histological findings of these two granulomatous disorders are similar.AIM To study the diagnostic accuracy of Xpert MTB/RIF Ultra(Xpert Ultra)and True-Nat MTB plus assay(TrueNat Plus)in the diagnosis of GITB diagnosis.METHODS We prospectively included patients suspected to have GITB who underwent colonoscopy and had endoscopic findings consistent with tuberculosis,such as ulcers,ulcerated strictures,and ulcero-polypoidal lesions.Xpert Ultra and True-Nat Plus assays were performed using standard protocols from intestinal tissue to assess the comparative performance of the two assays(Xpert Ultra and TrueNAT Plus)in diagnosing GITB compared with a composite reference standard(CRS).The CRS included a combination of clinical symptoms,tissue acid-fast bacilli smear/culture,imaging findings,histopathology,and response to therapy to diagnose GITB.RESULTS Of the 38 patients with complete follow-up,26 had GITB,and 12 served as controls(n=10 Crohn’s disease cases,n=2 alternate diagnosis).GITB cases included three acid-fast bacilli culture-positive patients,four with granulomas,17 with Xpert Ultra positivity and 15 with TrueNat plus positivity.Compared with the CRS,the overall sensitivity and specificity of Xpert Ultra for the diagnosis of GITB was 65.38%[95%confidence interval(CI):44.33-82.79]and 83.33%(95%CI:51.59-97.91),respectively.TrueNat plus had a sensitivity of 57.69%(95%CI:36.92-76.65)and specificity of 50%(95%CI:21.09-78.91).CONCLUSION TrueNat plus has a lower sensitivity and specificity compared with Xpert Ultra.However,the improved sensitivity of these tests compared with standard tests comes at the cost of reduced specificity. 展开更多
关键词 Gastrointestinal tuberculosis Crohn’s disease Inflammatory bowel disease Polymerase chain reaction Intestinal tuberculosis
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Unraveling the complex role of intestinal microbiota in drug permeability:Insights from N-acetylcysteine 认领 引用
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作者 Chutong Tian Zhonggui He 《Asian Journal of Pharmaceutical Sciences》 SCIE CAS CSCD 2026年第3期1-3,共3页
The Biopharmaceutics Classification System(BCS)serves as a foundational framework for drug development and,streamlines generic drugs approval by categorizing them based on solubility and intestinal permeability[1].How... The Biopharmaceutics Classification System(BCS)serves as a foundational framework for drug development and,streamlines generic drugs approval by categorizing them based on solubility and intestinal permeability[1].However,this system overlooks the influence of the intestinal microbiota on drug permeability. 展开更多
关键词 intestinal microbiota generic drugs drug permeability drug development biopharmaceutics classification system bcs serves foundational framework intestinal permeability howeverthis
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Construction of a risk prediction model for postoperative gastrointestinal dysfunction and prevention in patients with gastrointestinal tumors 认领 引用
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作者 Xiao-Hui Wang Yi Wang +3 位作者 Xi Liu Xiao-Lan Ouyang Fen Xie Lu Liao 《World Journal of Gastrointestinal Surgery》 SCIE 2026年第2期231-239,共9页
BACKGROUND The global incidence of gastrointestinal tumors is continuously increasing.Surgery remains the primary treatment modality.However,postoperative gastrointestinal dysfunction remains prevalent,severely impedi... BACKGROUND The global incidence of gastrointestinal tumors is continuously increasing.Surgery remains the primary treatment modality.However,postoperative gastrointestinal dysfunction remains prevalent,severely impeding patient recovery and increasing medical burden.Existing research investigating risk prediction and preventive management has some limitations.AIM To construct a risk-prediction model for postoperative gastrointestinal dysfunction in patients with gastrointestinal tumors and explore preventive management strategies.METHODS Data from 176 patients who underwent gastrointestinal tumor surgery at the authors’hospital between November 2022 and November 2024 were included.Patients were divided into groups according to Tilburg Frailty Scale scores on postoperative day 5.Risk factors were screened using univariate and multivariate logistic regression analyses to establish a model,and the effectiveness of preventive management measures was evaluated.RESULTS Seven factors including age,sex,body mass index,tumor stage,operative duration,and preoperative hemoglobin and albumin levels were identified as independent risk factors.The constructed model had an area under the receiver operating characteristic curve of 0.895.The incidence of postoperative gastrointestinal dysfunction in the intervention group was significantly lower than that in the control group using preventive management measures based on the model.CONCLUSION An effective risk-prediction model was constructed and independent risk factors were identified.Preventive management measures based on this model can reduce risk and provide a scientific basis for clinical practice. 展开更多
关键词 Gastrointestinal neoplasms Postoperative gastrointestinal dysfunction Risk prediction model Preventive management Intestinal barrier function
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Effects and mechanism of Bifidobacterium on intestinal inflammation resulting from deoxycholic acid-induced M1 polarization of macrophages 认领 引用 被引量：2
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作者 Peng-Chun Yang Chun-Yan Xiao +6 位作者 Jing Wang Cai-Hua Yan Qi-Yi Li Shi-Yu Li Jian Li Li-Jing Zhang Chi-Bing Dai 《World Journal of Gastroenterology》 SCIE CAS 2026年第6期77-96,共20页
BACKGROUND A high-fat diet(HFD)can cause systemic low-grade inflammation,metabolic and inflammatory diseases,and alter the composition of intestinal microbiota.Although probiotics mitigate intestinal inflammation,it i... BACKGROUND A high-fat diet(HFD)can cause systemic low-grade inflammation,metabolic and inflammatory diseases,and alter the composition of intestinal microbiota.Although probiotics mitigate intestinal inflammation,it is still unclear whether they can directly inhibit the production of deoxycholic acid(DCA)to prevent or alleviate intestinal inflammation.AIM To investigate changes in intestinal flora,fecal DCA levels,and cytokine profiles.METHODS Vancomycin was administered to significantly reduce the population of intestinal gram-positive bacteria,which helped in reducing the fecal DCA levels.Recruitment of pro-inflammatory macrophages,polarization of macrophages,and the inflammation associated with the intestinal flora of the HFD animal model were assessed.Their expression levels were analyzed through real-time polymerase chain reaction,immunofluorescence staining,liquid chromatography-mass spectrometry,and 16S rRNA high-throughput sequencing.RESULTS HFD or DCA promotes the infiltration of colon macrophages,causing their polarization toward the M1 phenotype.This polarization can be inhibited by both vancomycin and Bifidoba-cterium.Bifidobacterium enhances the species richness and uniformity of the intestinal microbiota in HFD mice;however,it does not improve these parameters in the presence of vancomycin.Bifidobacterium also does not increase the abundance of microbiota in HFD-fed or HFD-and-vancomycin-treated mice.HFD alters the relative abundance of intestinal microbiota at the phylum and genus levels.Bifidobacterium or vancomycin can partially mitigate these changes.CONCLUSION Bifidobacterium can inhibit HFD-induced intestinal inflammation or that resulting from DCA-induced M1 polarization of macrophages.It may also regulate bile acid levels and target cholesterol metabolism pathways,which may serve as potential therapeutic strategies for HFD-associated colitis. 展开更多
关键词 High-fat diet Bifidobacterium Deoxycholic acid Macrophage polarization Microbiota Intestinal inflammation
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Chitosan alleviates symptoms of Parkinson's disease by reducing acetate levels, which decreases inflammation and promotes repair of the intestinal barrier and blood–brain barrier 认领 引用 被引量：1
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作者 Yinying Wang Rongsha Chen +7 位作者 Guolin Shi Xinwei Huang Ke Li Ruohua Wang Xia Cao Zhongshan Yang Ninghui Zhao Jinyuan Yan 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第1期377-391,共15页
Studies have shown that chitosan protects against neurodegenerative diseases. However, the precise mechanism remains poorly understood. In this study, we administered chitosan intragastrically to an MPTP-induced mouse... Studies have shown that chitosan protects against neurodegenerative diseases. However, the precise mechanism remains poorly understood. In this study, we administered chitosan intragastrically to an MPTP-induced mouse model of Parkinson's disease and found that it effectively reduced dopamine neuron injury, neurotransmitter dopamine release, and motor symptoms. These neuroprotective effects of chitosan were related to bacterial metabolites, specifically shortchain fatty acids, and chitosan administration altered intestinal microbial diversity and decreased short-chain fatty acid production in the gut. Furthermore, chitosan effectively reduced damage to the intestinal barrier and the blood–brain barrier. Finally, we demonstrated that chitosan improved intestinal barrier function and alleviated inflammation in both the peripheral nervous system and the central nervous system by reducing acetate levels. Based on these findings, we suggest a molecular mechanism by which chitosan decreases inflammation through reducing acetate levels and repairing the intestinal and blood–brain barriers, thereby alleviating symptoms of Parkinson's disease. 展开更多
关键词 acetate adenosine 5′-monophosphate-activated protein kinase blood–brain barrier chitosan dopamine neurons inflammation intestinal barrier Parkinson's disease peroxisome proliferator-activated receptor delta short-chain fatty acids
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Prebiotic Microcapsule-Encapsulated Pterostilbene Alleviates Ulcerative Colitis by Regulating the Intestinal Microenvironment and Activating AHR/IL-22 Pathway 认领 引用 被引量：1
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作者 Huanyu Li Ziwei Yang +10 位作者 Chuanyu Zhang Xueyong Wei Wenjing Wang Ting Bai Zhichao Deng Bowen Gao Manli Cui Weixuan Jing Mingzhen Zhang Zhaoxiang Yu Mingxin Zhang 《Engineering》 SCIE EI CSCD 2026年第1期219-233,共15页
Ulcerative colitis(UC)is a chronic,non-specific inflammatory disorder of the intestines whose etiology is influenced by various factors.Intestinal barrier impairment due to disturbances in the intestinal microenvironm... Ulcerative colitis(UC)is a chronic,non-specific inflammatory disorder of the intestines whose etiology is influenced by various factors.Intestinal barrier impairment due to disturbances in the intestinal microenvironment is a key feature of UC.Current therapeutic strategies are constrained in their capacity to fully restore the intestinal barrier and achieve comprehensive resolution of inflammation in a coordinated manner.In this study,we constructed a pterostilbene(PSB)-loaded prebiotic microcapsule(PSB@MC)using a microfluidic electrospray method and characterized it using various means.Its safety,biodistribution,protective,and therapeutic effects on colitis were evaluated in various animal models.The potential mechanisms by which PSB@MC exerts its therapeutic effects were subsequently explored.The results indicated that PSB@MC exhibited favorable biocompatibility and facilitated targeted delivery of PSB to the colon.Moreover,the wrinkled morphology of PSB@MC contributed to prolonged drug retention in the colon.Oral PSB@MC administration restored intestinal microenvironment homeostasis by scavenging reactive oxygen species(ROS),decreasing pro-inflammatory cytokines,modulating gut microbiota and metabolism,and providing protective and therapeutic benefits against dextran sulfate sodium-induced colitis.Additionally,our research demonstrated that PSB@MC could activate the aryl hydrocarbon receptor/interleukin-22(AHR/IL-22)pathway to enhance the integrity of the intestinal barrier.These results suggest that PSB@MC could be a new,secure,and efficient UC therapy option. 展开更多
关键词 Ulcerative colitis Pterostilbene Prebiotic microcapsule Intestinal barrier AHR/IL-22 pathway
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Taurine suppresses gastric intestinal metaplasia in patient-derived organoids and Atp4a--mice 认领 引用
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作者 Ke Liu Xi Zhang +2 位作者 Fa-Zhan Li Peng-Yuan Zheng Yang Mi 《World Journal of Gastrointestinal Oncology》 SCIE 2026年第2期228-239,共12页
BACKGROUND Gastric intestinal metaplasia(GIM)represents a critical precancerous condition in the progression from chronic gastritis to gastric cancer,with limited therapeutic options.Emerging evidence suggests that ta... BACKGROUND Gastric intestinal metaplasia(GIM)represents a critical precancerous condition in the progression from chronic gastritis to gastric cancer,with limited therapeutic options.Emerging evidence suggests that taurine,a cytoprotective amino acid,may modulate gastric epithelial dysfunction.However,its application and efficiency in the context of GIM remain poorly understood.AIM To investigate the therapeutic effects of taurine on GIM using patient-derived organoids and Atp4a-/-mouse models.METHODS Patient-derived GIM organoids(n=3)and Atp4a-/-mice,which spontaneously develop GIM,were used as experimental models.Morphological changes were assessed via Alcian blue-periodic acid Schiff staining.The expression levels of the gastric epithelial marker mucin 5AC(MUC5AC)and GIM-associated markers(caudal type homeobox 2[CDX2],MUC2,Trefoil factor family 3[TFF3])were quantified via quantitative PCR,Western blotting,and immunohistochemistry.RESULTS We confirmed that taurine treatment significantly attenuated pathological changes,including glandular hypertrophy and vacuolar dilation,in Atp4a-/-mice.It also reduced GIM severity compared with that in the untreated model group.Under taurine treatment,MUC5AC expression was significantly increased,whereas the intestinalspecific markers CDX2,MUC2,and TFF3 were reduced(P<0.05).In parallel,in patient-derived GIM organoids,taurine treatment significantly ameliorated GIM features,as evidenced by increased MUC5AC expression and decreased CDX2,MUC2,and TFF3 expression.CONCLUSION This study highlights the potential application of taurine as a therapeutic agent for treating GIM,offering a promising strategy for its clinical management. 展开更多
关键词 Atp4a gastric intestinal metaplasia models Biomarkers Gastric intestinal metaplasia Organoid Taurine
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Analysis of histopathological and clinical prognostic factors in lymphomas involving the gastrointestinal system 认领 引用
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作者 Dilara Ozyigit Buyuktalanci Ebru Cakir +4 位作者 Betül Bolat Kucukzeybek Sultan Deniz Altindag Asu Fergun Yilmaz Hatice Demet Kiper Osman Nuri Dilek 《World Journal of Gastrointestinal Oncology》 SCIE 2026年第3期122-131,共10页
BACKGROUND Primary gastrointestinal lymphomas(PGIL)are rare tumors that can involve the whole gastrointestinal(GI)tract.Although lymphomas can originate from any part of the gastrointestinal tract,the most common site... BACKGROUND Primary gastrointestinal lymphomas(PGIL)are rare tumors that can involve the whole gastrointestinal(GI)tract.Although lymphomas can originate from any part of the gastrointestinal tract,the most common sites are the stomach,small intestine,and ileocecal region.AIM To examine the clinicopathologic and prognostic features of PGIL.METHODS We performed a retrospective single-center analysis of 111 patients diagnosed with gastrointestinal lymphomas(GIL)at Izmir Katip Celebi University Ataturk Training and Research Hospital.Histopathological,clinical,and prognostic para-meters,including pathological subtype,Helicobacter pylori infection,tumor stage,grade,Performance Score(PS),International Prognostic Index,lactate dehydrogenase(LDH)level,and treatment modality of PGILs(2006-2018),were retro-spectively analyzed using SPSS 25.0.RESULTS The study included 111 patients diagnosed with GIL.The median age was 66 years(60 males,51 females).Sites of involvement were stomach(67.5%),small bowel(18%),large bowelectum(12.6%),and pancreas(1.8%).Among 62 patients with primary GIL,49(79%)had diffuse large B-cell lymphoma(DLBCL),6(9.7%)had extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue,2(3.2%)had mantle cell lymphoma,2(3.2%)had unclassified B-cell lymphoma,and 2(3.2%)had T-cell lymphoma.The 1-,3-,and 5-year overall survival(OS)and event-free survival rates were 67%,56%,47%,and 80%,58.6%,54.4%,respectively.In univariate analysis,LDH level(LDH≥270 U/L)(P=0.029),PS[Eastern Cooperative Oncology Group(ECOG)≥2](P<0.0001),and surgical treatment(P=0.002)were associated with survival.In multivariate analysis,a poor PS(ECOG≥2)(P=0.010)was an independent predictor of poor OS.CONCLUSION In this study,the stomach was the most frequently involved site,DLBCL was the predominant subtype,and poor performance status was associated with poorer survival. 展开更多
关键词 Gastrointestinal system Lymphoma Gastric lymphoma Intestinal lymphoma
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Radiotherapy combined with bevacizumab in gastrointestinal cancers:Balancing efficacy against the risk of intestinal perforation 认领 引用
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作者 Yan Xu Xiao-Bing Huang Yong-Gang He 《World Journal of Radiology》 2026年第1期65-67,共3页
The combination of radiotherapy with bevacizumab represents a promising therapeutic strategy for advanced gastrointestinal cancers.While this combination leverages synergistic mechanisms to enhance antitumor efficacy,... The combination of radiotherapy with bevacizumab represents a promising therapeutic strategy for advanced gastrointestinal cancers.While this combination leverages synergistic mechanisms to enhance antitumor efficacy,it also poses significant safety concerns,particularly regarding the risk of intestinal perforation.This letter discusses the current understanding of this dual effect and underscores the importance of careful patient selection,advanced radiotherapy techniques,and vigilant toxicity monitoring to optimize clinical outcomes. 展开更多
关键词 Radiotherapy Bevacizumab Gastrointestinal cancers Intestinal perforation Combination therapy Toxicity management
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A new synbiotic supplementation ameliorates ulcerative colitis via modulating microbial homeostasis,protecting intestinal barrier integrity,and maintaining immunity homeostasis in mice 认领 引用
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作者 Yongbo Kang Liping Li +2 位作者 Jing Guo Yue Cai Ying Yang 《Food Science and Human Wellness》 SCIE CAS CSCD 2026年第4期1774-1810,共37页
Ulcerative colitis(UC)is established by a chronic,diffuse inflammation of colonic mucosa with poorly defined etiology,and without sufficient treatment or cure available for remission.In this context,there is a growing... Ulcerative colitis(UC)is established by a chronic,diffuse inflammation of colonic mucosa with poorly defined etiology,and without sufficient treatment or cure available for remission.In this context,there is a growing recognition and consensus that synbiotic supplement may be promising and impactful strategies towards ameliorating UC and related inflammatory disorders,garnering significant attention from researchers as an alternative therapy.Herein,we innovatively prepared a novel synbiotic combination including Lactobacillus acidophilus,Bifidobacterium infants and prebiotics konjac glucomannan oligosaccharides(KGMO)to explore the potential therapeutic effects in dextran sodium sulfate(DSS)induced UC mouse model.The results demonstrated that the synbiotic effectively improved colitis symptoms in mice by mitigating weight loss,disease activity index(DAI),colonic pathological damage,and colonic oxidative stress.it also observed that the synbiotic preserve intestinal barrier function integrity,reduces metabolic endotoxemia as well as inhibits the TLR4/NF-κB,NLRP3/Caspase-1,and Nrf2/Keap1 signaling pathway.Furthermore,the synbiotic modulated microbial homeostasis directly by enhancing beneficial microbes and reducing potentially harmful bacteria.In addition,microbiome phenotype prediction and bacterial functional potential prediction analysis demonstrated that the synbiotic supplementation regulated gut microbiota function involving inflammatory injury,metabolism,immune response,and pathopoiesia.Especially,the synbiotic not only restored the balance of Th1/Th2 cells as well as Th17/Treg cells along with specific inflammatory factors expression,but also maintained bile acid homeostasis by regulating FXR/FGF15 signaling pathway.Especially important is that the synbiotic was as effective as mesalazine against UC.According to above data,it is seen that this novel synbiotic could be a good candidate drug for ameliorating UC through its anti-inflammatory,antioxidant stress,antipyroptosis properties,regulation of bile acid metabolism,and remission of endothelial dysfunction and gut dysbiosis. 展开更多
关键词 Synbiotic Ulcerative colitis Gut microbiota Intestinal permeability Inflammation Oxidative stress Pyroptosis Bile acid homeostasis
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Lactate alleviates intestinal barrier injury in weaned piglets via activation of the Wnt/β-catenin pathway and promotion of intestinal epithelial cell proliferation 认领 引用
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作者 Mingyu Wang Yifan Chen +10 位作者 Jiaojiao Chen Aimin Wu Daiwen Chen Bing Yu Jun He Jie Yu Xiangbing Mao Zhiqing Huang Yuheng Luo Junqiu Luo Ping Zheng 《Journal of Animal Science and Biotechnology》 SCIE CAS CSCD 2026年第1期443-456,共14页
Background Inflammatory bowel disease causes intestinal structural damage,impairs gut function,hinders animal growth and development,and reduces farming efficiency.Previous studies demonstrated that lactate alleviates... Background Inflammatory bowel disease causes intestinal structural damage,impairs gut function,hinders animal growth and development,and reduces farming efficiency.Previous studies demonstrated that lactate alleviates dextran sulfate sodium(DSS)-induced inflammation and mitigates weight loss by enhancing intestinal barrier functions.However,the mechanisms underlying lactate-mediated protection of the intestinal epithelial barrier remain unclear.This study aimed to explore the protective effect of lactate on intestinal barrier damage in colitis piglets and the possible underlying mechanisms through in vivo and in vitro experiments.Methods A total of 6021-day-old weaned female piglets were randomly assigned into three groups based on weight:the control group(basal diet with physiological saline gavage),the DSS group(basal diet with 5%DSS gavage),and the DSS+LA group(2%lactate diet with 5%DSS gavage).There were 10 replicates per treatment,with 2 piglets per replicate.Jejunal morphology was assessed via hematoxylin and eosin staining,while Western blotting quantified the protein levels of proliferation markers,including cluster of differentiation 24(CD24),cyclin D1,and wingless/integrated(Wnt)/β-catenin signaling components.In vitro,0.08%DSS and 2–32 mmol/L sodium lactate-treated intestinal porcine epithelial cell line-J2(IPEC-J2)cells(n=4)were assessed for viability(Cell Counting Kit-8 assay),apoptosis(flow cytometry),and proliferation parameters,including cell cycle analysis and Leucine-rich repeat-containing G-protein coupled receptor 5(Lgr5+)stem cell quantification.Results In vivo,DSS administration induced jejunal villus shortening(P<0.05),downregulated protein levels of CD24,cyclin D1,casein kinase 1(CK1),and dishevelled-2(DVL2)(P<0.05).In vitro,DSS promoted apoptosis,inhibited proliferation,diminished the Lgr5+cell populations(P<0.05),and reduced S-phase cell proportions(P<0.05).Conversely,lactate supplementation ameliorated DSS-induced villus atrophy(P<0.05),restored CD24,cyclin D1,CK1,and DVL2 protein levels(P<0.05).Furthermore,in vitro,sodium lactate attenuated DSS-induced apoptosis(P<0.05),enhanced IPEC-J2 proliferation(P<0.05),expanded Lgr5+cells(P<0.05),and increased S-phase progression(P<0.05).Conclusions In summary,lactate ameliorated intestinal barrier damage in DSS-induced colitis by activating the Wnt/β-catenin pathway and restoring the balance between epithelial cell proliferation and apoptosis.This study provides novel mechanistic evidence supporting lactate's therapeutic potential for IBD management. 展开更多
关键词 Apoptosis Intestinal inflammation Lactate Lgr5 Piglets Proliferation Wnt/β-catenin pathway
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Mitofusin 2 is required for preventing deoxynivalenol-induced porcine intestinal epithelial cell damage 认领 引用
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作者 Kan Xiao Minfang Zhang +7 位作者 Qingqing Lv Feifei Huang Qilong Xu Junjie Guo Jiangchao Zhao Huiling Zhu Shaokui Chen Yulan Liu 《Journal of Animal Science and Biotechnology》 SCIE CAS CSCD 2026年第1期376-387,共12页
Backgrounds Deoxynivalenol(DON)is an abundant environmental pollutant in feed,posing serious health hazards to animals.However,whether DON triggers an imbalance in mitochondrial fission/fusion and the underlying mecha... Backgrounds Deoxynivalenol(DON)is an abundant environmental pollutant in feed,posing serious health hazards to animals.However,whether DON triggers an imbalance in mitochondrial fission/fusion and the underlying mechanisms involved remain poorly understood.Our aim was to clarify whether mitochondrial fission or fusion proteins participated in DON-caused intestinal damage in pigs.Methods Firstly,two groups of weaning pigs were fed a basal diet,or basal diet supplemented with 4 mg DON/kg for 3 weeks.Additionally,another two groups of weaning pigs were given an oral gavage with 2 mg/kg body weight DON or an equivalent amount of normal saline.In addition,the involvement of mitochondrial fission or fusion proteins in DON-induced intestinal damage was further verified in intestinal porcine epithelial cell line(IPEC-1)by overexpressed plasmids of dynamin related protein 1(Drp1)and mitofusin 2(Mfn2)which were determined by animal studies.Finally,a mitochondrial fusion promotor M1 was used in IPEC-1 cells to explore the role of Mfn2 in DON-induced intestinal damage.Results Dietary DON caused jejunal damage and inflammation,reduced intestinal Drp1,mitofusin 1(Mfn1)and Mfn2,and induced cell apoptosis.DON gavage also impaired jejunal structure and led to decreased Drp1 and Mfn2,and increased cell apoptosis.Moreover,DON challenge also resulted in cell damage and mitochondrial dysfunction,accompanied by abnormal protein expression of mitochondrial fission/fusion proteins and increased cell apoptosis in IPEC-1 cells.Subsequently,Mfn2,but not Drp1 overexpression plasmid restored mitochondrial fission/fusion protein expression,suppressed cell apoptosis,mitigated cell damage and mitochondrial dysfunction in IPEC-1 cells after DON challenge.Finally,M1 alleviated DON-induced reduction of Mfn2 protein and cell apoptosis,rescued mitochondrial dysfunction,barrier function impairment and cell damage.Conclusions Overall,our study demonstrates that DON exposure triggers Mfn2 protein dysregulation,which in turn mediates DON-induced intestinal epithelial damage in piglets. 展开更多
关键词 Deoxynivalenol Intestinal injury Mfn2 Mitochondrial homeostasis Piglets
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Polystyrene microplastics exposure increases the disruption of intestinal barrier integrity and gut microbiota homeostasis during obesity and aging 认领 引用
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作者 Gang Wei Wangrui Liu +4 位作者 Fengjie Shen Rongrong Xie Fengwei Wang Huaqi Guo Lin Liu 《Journal of Environmental Sciences》 SCIE EI CAS CSCD 2026年第4期430-443,共14页
The global rise in intestinal dysfunction has been linked to modifiable risk factors including high-fat diet(HFD)-induced obesity/diabetes,microplastics(MPs)and aging,yet their combined effects remain unclear.This stu... The global rise in intestinal dysfunction has been linked to modifiable risk factors including high-fat diet(HFD)-induced obesity/diabetes,microplastics(MPs)and aging,yet their combined effects remain unclear.This study examined the combined effects of chronic low dose polystyrene MPs(∼25μg/(kg・day))with HFD or aging on intestinal barrier function in C57BL/6 J mice over 14 weeks.Juvenile mice receiving either normal chow(NCD)or HFD,along with aged NCD-fed mice,were subjected to MPs exposure.Results demonstrated that MPs exposure or HFD feeding(and aging)significantly exacerbated the pathological changes developed in colon tissues of mice relative to those of control mice,including gut permeability,oxidative stress,pro-inflammatory response and apoptosis.Moreover,combination of MPs exposure with HFD feeding(and aging)further potentiated the harmful effects on colon dysfunctions,clearly showing a synergistic deterioration effect(‘double hit’).More importantly,we found that the recovery of colon damages resulting from MPs exposure and HFD feeding was disrupted after their withdrawal,leading to the worse effects on gut microbiota dysbiosis and intestinal function.Furthermore,oral administration of Akkermansia muciniphila prevented intestinal barrier dysfunction and decreased intestinal permeability from MPs exposure and HFD feeding co-exposure.Our findings in this study emphasized the important role of avoiding MPs exposure in the prevention and treatment of intestinal-related dysfunctions,and provided potential therapeutic approaches.The oral administration of gut microbiota,such as Akkermansia muciniphila,contributed to restoration of intestinal barrier function,uncovering a new landscape for treating intestinal disabilities caused by MPs exposure. 展开更多
关键词 Microplastics Metabolic disorder Intestinal permeability Colonic microbiota dysbiosis
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Bioengineered intestinal models:structural precision drives functional and microbial fidelity 认领 引用
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作者 Ziqi Gao Huilong Du +7 位作者 Shuyuan Yu Qi Li Yang Li Jun Yin Huayong Yang Yue Wang Hongzhao Zhou Luqi Shen 《Bio-Design and Manufacturing》 SCIE EI CAS CSCD 2026年第2期240-265,I0004,共26页
The intestine is a key component of the barrier,absorption,and immune systems,contributing significantly to maintaining internal homeostasis and influencing disease progression.Its distinctive physiological functions ... The intestine is a key component of the barrier,absorption,and immune systems,contributing significantly to maintaining internal homeostasis and influencing disease progression.Its distinctive physiological functions arise from a complex interplay between its structure and microenvironment.Recent advancements in bioengineering technologies now enable the construction of in vitro intestinal models that faithfully recapitulate the organizational and functional characteristics of native tissue.This review examines the interface between in vitro models and native intestinal biology,offering insights into the replication of organ functions from a manufacturing perspective.We explore bioengineering strategies that enable the mapping of cross-scale structures and the creation of biomimetic environments essential for physiological performance.Furthermore,we discuss pragmatic optimization strategies for applying these models to both physiological and pathological studies,thereby enhancing their translational potential for drug development,disease modeling,and personalized medicine.In contrast to previous reviews,this work proposes an engineering-centered framework for linking structural fabrication strategies to functional performance across intestinal model types. 展开更多
关键词 Intestinal model Organ-on-chip Organoid 3 D bioprinting Biomedical application
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Electroacupuncture Alleviates Pulmonary and Intestinal Injury in Septic Mice via Inhibiting NLRP3 Inflammasome and Remodeling Gut Microbiota 认领 引用
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作者 Xiao-lei Zhang Hai-ming Hu +5 位作者 Qun-feng Yao Xiong-jie Sun Xiao-wei Yao Lu Cao Jun Ma Hong-tao Liu 《Current Medical Science》 SCIE CAS CSCD 2026年第1期143-160,共18页
Objective Electroacupuncture(EA)has emerged as a clinically adopted complementary modality in the management of res-piratory and digestive disorders.This investigation sought to elucidate the therapeutic potential of ... Objective Electroacupuncture(EA)has emerged as a clinically adopted complementary modality in the management of res-piratory and digestive disorders.This investigation sought to elucidate the therapeutic potential of EA against sepsis-induced pulmonary and gastrointestinal injuries,with particular emphasis on delineating its multimodal mechanistical pathways.Methods Sepsis was induced in C57BL/6 mice by administeringting lipopolysaccharide(LPS)one hour after EA interven-tion at the Zusanli(ST36)and Tianshu(ST25)acupoints for eight days.Inflammatory responses and barrier function were evaluated in the lung and colon tissues.Hematoxylin and Eosin(H&E)staining was performed on lung tissues,while colon tissues were subjected to H&E staining,Wheat Germ Agglutinin-Fluorescein Isothiocyanate(WGA-FITC)staining,and Alcian Blue staining.Additionally,Quantitative Real-Time Polymerase Chain Reaction(qRT-PCR)and Western blotting were used to explore potential molecular mechanisms.Furthermore,16S rRNA gene sequencing was employed to analyze changes in the gut microbiota.Results EA ameliorated both pulmonary injury and intestinal damage in septic mice.This protective effect was mediated through significant attenuation of pulmonary and intestinal inflammation,coupled with partial restoration of gut microbiota homeostasis.Specifically,EA inhibited the activation of Nod-like receptor thermal protein domain associated protein 3(NLRP3)inflammasome and mitogen-activated protein kinase(MAPK)pathways,and upregulated the transcription of lung barrier-related factors(MMP2,MMP9,Occludin)in the lung.In addition,EA improved inflammation and reduced damage to the intestinal mucosal barrier in the colon.This was accomplished by decreasing the expression of pro-inflammatory cytokines(IL-1β,TNF-α)and increasing the levels of mucin and glycoproteins.Furthermore,EA intervention altered the structure of the gut microbiota,resulting in a significant increase in the abundance of beneficial bacteria,such as Rumino-coccaceae and Roseburia.Conclusion EA is a potential adjunct therapy for sepsis-related pulmonary and intestinal injury.The mechanism involves the inhibition of the NLRP3 inflammasome and remodeling of the gut microbiota. 展开更多
关键词 Electroacupuncture Sepsis Acute lung injury Intestinal barrier dysfuntion Gut microbiota NLRP3 inflammation MAPK signaling
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Multi-omic analysis for dietary supplementation of different ratios of soluble and insoluble fiber on intestinal microbiota,metabolites and inflammation of weaned piglets 认领 引用
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作者 Yetong Xu Chengyu Zhou +7 位作者 Yingying Lu Xutong Guo Minyue Zong Junwei Zhu Pan Zhou Jiaman Pang Xie Peng Zhihong Sun 《Journal of Integrative Agriculture》 SCIE CAS CSCD 2026年第4期1606-1618,共13页
Different types of dietary fiber(DF)play important roles in enhancing intestinal health and overall performance in animals.This study investigated the effects of high-DF diets containing different ratios of soluble to... Different types of dietary fiber(DF)play important roles in enhancing intestinal health and overall performance in animals.This study investigated the effects of high-DF diets containing different ratios of soluble to insoluble dietary fiber(SDF:IDF)on growth performance,intestinal barrier integrity,microbiota,and metabolite profiles in weaned piglets.The four dietary treatments consisted of a basal diet(CON)and three high-DF diets with SDF:IDF ratios of 0.37,0.25,and 0.13(designated HF-0.37,HF-0.25,and HF-0.13,respectively).On days 14 and 28,colonic tumor necrosis factor-α,interleukin-1β,interleukin-6,and interleukin-8 concentrations were higher in the HF-0.37 group than in the CON,HF-0.25,and HF-0.13 groups(P<0.05).Plasma D-lactate and endotoxin levels were lower in the HF-0.25 group compared to the CON group at both time points(P<0.05).Furthermore,colonic zonula occludens 1 expression was upregulated in the HF-0.25 and HF-0.13 groups compared to the CON and HF-0.37 groups on day 14(P<0.05).At the transcriptional level,all three high-DF diets modulated signaling pathways associated with inflammation and immune responses in the colon.Notably,DF supplementation particularly the HF-0.25 diet upregulated colonic levels of 3-indole butyric acid,nicotinic acid,and 3-methylthiopropylamine on d 14 and reduced certain peptide levels by d 28.These findings indicate that DF supplementation,especially at an SDF:IDF ratio of 0.25,exerts beneficial effects on intestinal integrity in weaned piglets,potentially mediated by alterations in colonic metabolite profiles,whereas HF-0.37 and HF-0.13 exhibited limited impacts on intestinal barrier function. 展开更多
关键词 weaned piglets soluble fiber insoluble fiber multi-omics intestinal integrity
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Reuterin-producing Limosilactobacillus reuteri with glycerol metabolism ameliorates Staphylococcus aureus-induced intestinal inflammation and dysfunction without gut microbiota dependent 认领 引用
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作者 Jinmei Li Kaixiang Zou +4 位作者 Xinrui Li Ke Zhu Yijuan Li Hua Wei Zhihong Zhang 《Food Science and Human Wellness》 SCIE CAS CSCD 2026年第2期823-835,共13页
Limosilactobacillus reuteri is a vertebrate symbiont that is widely appreciated as being of significant ecological importance for human health.As a unique feature,L.reuteri converts glycerol to the antimicrobial compo... Limosilactobacillus reuteri is a vertebrate symbiont that is widely appreciated as being of significant ecological importance for human health.As a unique feature,L.reuteri converts glycerol to the antimicrobial compound reuterin using enzymes encoded in its propanediol-utilization operon and evolves with host-driven diversification.Reuterin-producing L.reuteri HLRE13 was selectively isolated from poultry previously and confirmed to inhibit the growth of Staphylococcus aureus in vitro.However,it remains unclear whether L.reuteri HLRE13 retains these antagonistic properties when ingested in specific-pathogen-free mice.Here,we investigated the ameliorative effects and potential mechanisms of action of L.reuteri HLRE13 in combination with glycerol on S.aureus-induced infection phenotypes in mice.Firstly,our results confirmed that L.reuteri HLRE13 effectively inhibited the intestinal colonization of S.aureus CMCC26003;Secondly,L.reuteri HLRE13 combined with glycerol could alleviate the intestinal tissues damage caused by S.aureus through increasing the expression of ZO-1,Occludin,and MUC-2,ameliorate the intestinal systemic inflammatory response,and maintain the balance of gut microbiota by increasing the relative abundance of Lactobacillus and reducing the relative abundance of Staphylococcus.Furthermore,the colonization resistance was also found on L.reuteri HLRE13 combined with glycerol against S.aureus in pseudo germ-free mice,and they exerted the similar effects on alleviating intestinal damage and improving immune function.Combining these results,we speculate that reuterin-producing L.reuteri antagonize S.aureus in mice without the gut microbiota-dependent manner.Overall,our findings will provide a theoretical foundation for the scientific cognition of L.reiteri in maintaining intestinal health by producing reuterin. 展开更多
关键词 Limosilactobacillus reuteri Glycerol Reuterin Colonization resistance Intestinal barrier Gut microbiota
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High-lipid diets exacerbate copper-induced hepatointestinal toxicity in yellow catfish(Pelteobagrus fulvidraco)via gut microbiota dysbiosis 认领 引用
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作者 Lei Wang Heng Wang +2 位作者 Xuan Xue Chang Gao Yunzhi Yan 《Journal of Environmental Sciences》 SCIE EI CAS CSCD 2026年第6期729-740,共12页
Copper(Cu)-contained chemicals and high-lipid diets are commonly applied in aquaculture, both of them are capable of negatively affecting fish health via complicated mechanisms, yet their microbiota-mediated interacti... Copper(Cu)-contained chemicals and high-lipid diets are commonly applied in aquaculture, both of them are capable of negatively affecting fish health via complicated mechanisms, yet their microbiota-mediated interactions remain unclear. This study investigated their combined effects on yellow catfish(Pelteobagrus fulvidraco). A control(Con), high-lipid(HL), and HL + antibiotics(HLA, deplete intestinal microbiota) diets were fed fish for nine weeks, and half fish underwent acute Cu exposure(0.8 mg/L) during week nine(assigned as ConCu, HLCu,and HLACu, respectively). Results showed the HL feeding impaired growth but not Cu exposure. The HL and HLA groups showed exacerbated hepatic vacuolization, oxidative stress(reduced antioxidant enzymes, elevated malondialdehyde(MDA), and inflammation(upregulated tnfα, il1β, and nfκb expression). Cu exposure worsened these effects in all groups, further reducing intestinal villus length and tight junction genes(zo1 and occludin)expression while activating mitogen-activated protein kinase(MAPK)-related inflammation. Hepatic Cu accumulation followed HLACu > HLCu > ConCu(P < 0.05), linked to upregulated Cu transporters(ctr1 and ctr2) and metallothionein(mt2) expression. Microbiota analysis revealed high-lipid diet and Cu exposure caused microbiota dysbiosis, reducing Plesiomonas and Pseudomonas abundances, which amplified copper toxicity. This study demonstrates that high-lipid diets intensify Cu-induced hepatointestinal toxicity via oxidative and inflammatory pathways and microbiota dysbiosis, highlighting microbiome-driven Cu metabolism as a key mechanism in fish toxicity. 展开更多
关键词 High lipid diet Copper exposure Liver damage Intestinal microbiota
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