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Reducing agents for induction and maintenance therapy achieve long-term remission of refractory ulcerative colitis:A case report and review of literature 认领 引用
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作者 Pamela B Sylvestre 《World Journal of Gastroenterology》 SCIE CAS 2026年第2期152-161,共10页
BACKGROUND Ulcerative colitis(UC)is a chronic and debilitating inflammatory bowel disease.Cumulative evidence indicates that excess hydrogen peroxide,a potent neutrophilic chemotactic agent,produced by colonic epithel... BACKGROUND Ulcerative colitis(UC)is a chronic and debilitating inflammatory bowel disease.Cumulative evidence indicates that excess hydrogen peroxide,a potent neutrophilic chemotactic agent,produced by colonic epithelial cells has a causal role leading to infiltration of neutrophils into the colonic mucosa and subsequent development of UC.This evidence-based mechanism identifies hydrogen peroxide as a therapeutic target for reducing agents in the treatment of UC.CASE SUMMARY Presented is a 41-year-old female with a 26-year history of refractory UC.Having developed steroid dependence and never achieving complete remission on treatment by conventional and advanced therapies,she began treatment with oral R-dihydrolipoic acid(RDLA),a lipid-soluble reducing agent with intracellular site of action.Within a week,rectal bleeding ceased.She was asymptomatic for three years until a highly stressful experience,when she noticed blood in her stool.RDLA was discontinued,and she began treatment with oral sodium thiosulfate pentahydrate(STS),a reducing agent with extracellular site of action.After a week,rectal bleeding ceased,and she resumed oral RDLA and discontinued STS.To date,she remains asymptomatic with normal stool calprotectin while on RDLA.CONCLUSION STS and RDLA are reducing agents that serve as highly effective and safe therapy for the induction and maintenance of remission in UC,even in patients refractory or poorly controlled by conventional and advanced therapies.Should preliminary findings be validated by subsequent clinical trials,the use of reducing agents could potentially prevent thousands of colectomies and represent a paradigm shift in the treatment of UC. 展开更多
关键词 Ulcerative colitis Colitis Inflammatory bowel disease Hydrogen peroxide Sodium thiosulfate R-dihydrolipoic acid Reducing agent Redox homeostasis Reactive oxygen species Case report
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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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Electroacupuncture at ST36 protects against dextran sulfate sodium-induced ulcerative colitis in mice by enhancing sympathetic nerve innervation in colonic tissue 认领 引用
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作者 Dongfeng Zhao Yuquan Yang +8 位作者 Junhao Liang Chuanglong Xu Chunlan Tang Mingming Zhang Chenguang Li Yongjian Zhao Bing Shu Wei Gou Yongjun Wang 《MedScience》 SCIE CAS CSCD 2026年第1期164-172,共9页
Ulcerative colitis(UC),characterized by diffuse colonic inflammation and enteric nervous system(ENS)alterations,remains a therapeutic challenge.While the role of the parasympathetic nervous system in intestinal inflam... Ulcerative colitis(UC),characterized by diffuse colonic inflammation and enteric nervous system(ENS)alterations,remains a therapeutic challenge.While the role of the parasympathetic nervous system in intestinal inflammation has been extensively documented,understanding of sympathetic nervous system(SNS)function in UC pathogenesis remains limited.Electroacupuncture(EA)at ST36(Zusanli)is a widely used alternative therapy for UC,yet its regulatory effects on the ENS-—particularly the SNS—and the underlying mechanisms remain unclear.Here,we established a 2.5%dextran sulfate sodium(DSS)-induced murine UC model and validated disease phenotypes via histological assessment.Using a non-anesthetic EA intervention protocol mimicking the clinical conditions,we found that EA at ST36 attenuated local inflammatory progression in DSS-induced UC mice and mitigated ENS degeneration.Critically,our results demonstrated that EA at ST36 specifically reversed SNS reduction(tyrosine hydroxylase-positive,TH+neurons)in colonic tissue caused by intestinal inflammation.In conclusion,this study reveals that EA at ST36 restores colonic homeostasis through a sympathetic-dependent mechanism,providing novel insights and therapeutic strategies for the clinical management of UC. 展开更多
关键词 electroacupuncture ST36(Zusanli) anti-inflammation ulcerative colitis sympathetic nerve systems
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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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Characteristics of gut microbiota and metabolites in patients with ulcerative colitis with fatigue 认领 引用
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作者 Zi-Xuan Liu Xiao-Yan Liu +4 位作者 Wei-Wei Tan Wei-Bing Zhang Ya-Li Zhang Lie Zheng Yan-Cheng Dai 《World Journal of Gastroenterology》 SCIE CAS 2026年第3期103-127,共25页
BACKGROUND Ulcerative colitis(UC)is a chronic,non-specific inflammatory bowel disease.The gut microbiome undergoes significant changes in UC.Fatigue is a highly prevalent and debilitating extraintestinal symptom of UC... BACKGROUND Ulcerative colitis(UC)is a chronic,non-specific inflammatory bowel disease.The gut microbiome undergoes significant changes in UC.Fatigue is a highly prevalent and debilitating extraintestinal symptom of UC,which negatively affects quality of life.However,its relationship with gut microbes and metabolites remains unclear.AIM To assess the gut microbiota and metabolomic characteristics of patients with UC with fatigue(HUCF).METHODS A total of 120 participants were recruited and divided into four groups(n=30 per group)based on the diagnosis of UC and Fatigue Scale-14 scores:HUCF,UC without fatigue(HUCN),healthy with fatigue(HHF),and healthy without fatigue(HHN).Fresh stool samples were collected for 16S rRNA sequencing and untargeted metabolomic analysis.RESULTS Metabolomic analysis revealed significant differences among the four groups(principal component analysis/partial least squares discriminant analysis,P=0.001),with differential expression of metabolites such as linoleoyl ethanolamide,arachidonoyl ethanolamide,glycocholic acid,and thromboxane(TX).Notably,TX was detected only in the HUCF group.Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis revealed alterations in eicosanoid,tryptophan,and tyrosine metabolism in the HUCF group.Microbial richness and diversity were significantly lower in the HUCF group than in the other three groups.The HUCF group showed enrichment of Hyphomicrobiales,Brucella,Eisenbergiella,Pediococcus,and Sellimonas.The HUCN group showed enrichment of Campylobacter-related taxa.The HHF group showed enrichment of Fusobacterium,Desulfovibrionaceae,and Bilophila.The HHN group showed enrichment of beneficial genera such as Adlercreutzia.Notably,Anaerococcus,a beneficial genus,was enriched in the HUCF group.Correlation analysis indicated that specific microbes(e.g.,Faecalibacterium and Escherichia-Shigella)were associated with the severity of UC and fatigue.CONCLUSION Patients with HUCF exhibit a distinct gut microbial structure and metabolomic profile.The pro-inflammatory metabolite TX and the genus Anaerococcus are uniquely enriched in patients with HUCF,suggesting their potential roles in the development of HUCF.These findings provide novel insights and a theoretical basis for improving the clinical management of HUCF. 展开更多
关键词 Ulcerative colitis Fatigue Gut Microbiota Metabolites Thromboxane Anaerococcus
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Enterococcus hirae QT4713 alleviated DSS-induced colitis by modulating gut microbiota and tryptophan metabolism in mice 认领 引用
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作者 Xueni Fan Zhenjiang Liu +7 位作者 Wei Liu Diantong Li Tingting Zhao Dongxu Wen Xin Li Qi Wang Bin Li Xiaodan Huang 《Food Science and Human Wellness》 SCIE CAS CSCD 2026年第4期1905-1919,共15页
Probiotics are known to alleviate inflammatory bowel disease,and their precise mechanisms remain unclear.In this study,we identified a strain of Enterococcus hirae QT4713,isolated from the Tibetan plateau,that exhibit... Probiotics are known to alleviate inflammatory bowel disease,and their precise mechanisms remain unclear.In this study,we identified a strain of Enterococcus hirae QT4713,isolated from the Tibetan plateau,that exhibited high anti-inflammatory activity in vitro.After confirming its tolerance to gastrointestinal fluids and safety,we evaluated the effect of E.hirae QT4713 on IBD using a dextran sulfate sodium(DSS)-induced colitis mouse model and analyzed the microbial response through metagenomic and metabolomics.The results indicated that E.hirae QT4713 alleviated colitis symptoms by reducing oxidative stress in the serum and inflammatory cytokine levels in colonic tissue,particularly IL-1β(P<0.05).It also reduced structural damage,inflammatory infiltration,and epithelial cell apoptosis in the colon.Additionally,the strain increased the expression of MUC-2 and occludin in colonic tissue,which helped to protect the colonic barrier.Furthermore,intervention with E.hirae QT4713 enriched beneficial bacteria such as Bifidobacteria and Lactobacillus,increased the levels of butyric acid and propionic acid in the gut(P<0.05),regulated tryptophan metabolism,and promoted the production of its indole derivatives,including 3-indoleacetonitrile,3-indoleacrylic acid,and indole-3-lactic acid(P<0.05),thus alleviating colitis.These findings provide new insights into how probiotics,such as E.hirae QT4713,alleviated colitis in a gut microbiotaryptophan metabolism-dependent manner. 展开更多
关键词 Probiotic Anti-inflammatory Colitis Gut microbiota Tryptophan metabolism
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Nanoplastics and triclosan co-exposure aggravates DSS-induced colitis in mice by interfering with Akkermansia muciniphila and tryptophan metabolism 认领 引用
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作者 Mengxing Cui Shilin Chen +16 位作者 Zhihan Zhang Yongjiang Yu Yingxi Xu Ludi Liu Huan Gao Xiaoyu Chen Ziqi Liu Xue Zhang Wenke Yuan Shen Chen Daochuan Li Liping Chen Xiumei Xing Yongmei Xiao Wen Chen Yan Liu Qing Wang 《Journal of Environmental Sciences》 SCIE EI CAS CSCD 2026年第3期189-200,共12页
The global incidence of inflammatory bowel disease(IBD)has been escalating.Recent studies have identified co-exposure to polystyrene nanoplastics(PSNP)and triclosan(TCS),two prevalent environmental pollutants,as emerg... The global incidence of inflammatory bowel disease(IBD)has been escalating.Recent studies have identified co-exposure to polystyrene nanoplastics(PSNP)and triclosan(TCS),two prevalent environmental pollutants,as emerging risk factors for IBD.However,the molecular mechanisms contributing to its deteriorative effect remain elusive.To explore the mechanisms,we conducted an integrative analysis of metagenomic and metabolomic data in a mouse model of colitis induced by dextran sulfate sodium(DSS)following co-exposure to PSNP and TCS.Results demonstrated that co-exposure to PSNP and TCS significantly exacerbated DSS-induced colitis,as evidenced by elevated disease activity indices and pro-inflammatory cytokine levels.Mechanistically,this aggravation correlated with a marked reduction in Akkermansia muciniphila abundance,which was further associated with the disruption of tryptophan metabolism.Specifically,the disruption of this metabolic pathway led to decreased production of two key tryptophan-derived metabolites:indole acetic acid(IAA)and indole acetamide(IAM).In-vitro experiments confirmed that co-exposure to PSNP and TCS inhibited the growth of A.muciniphila rather than affecting the integrity of intestinal epithelial cells.Additionally,IAA and IAM reduced inflammatory cytokine secretion in THP-1 cells.These findings suggest that the reduction in A.muciniphila abundance might decrease the production of IAA and IAM by disrupting tryptophan metabolism.This disruption ultimately contributes to the inflammatory response induced by co-exposure to PSNP and TCS.Our study offers a novel insight into microbiota-host interactions and potential therapeutic targets for intestinal disease. 展开更多
关键词 Nanoplastics Triclosan Colitis Gut microbiota Tryptophan metabolism
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An opposite pH-responsiveness“gating”strategy:Intelligent sporopollenin exine armor for targeted therapy of colitis 认领 引用
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作者 Jun Liu Zifang Ding +7 位作者 Jianxiong Wei Yuanqing Li Xiaoqing Wang Xiaodan Yan Dan Li Tiantian Ye Shujun Wang Jin Sun 《Asian Journal of Pharmaceutical Sciences》 SCIE CAS CSCD 2026年第3期202-218,共17页
Conventional therapy for ulcerative colitis(UC)is often limited by insufficient colonic targeting,short local retention and poor cellular drug uptake at lesion sites.Here,we develop a biomimetic colon-targeted deliver... Conventional therapy for ulcerative colitis(UC)is often limited by insufficient colonic targeting,short local retention and poor cellular drug uptake at lesion sites.Here,we develop a biomimetic colon-targeted delivery system based on an opposite pH-responsive“gating”strategy.Chrysanthemum sporopollenin(spo)microcapsules with a characteristic spiny architecture serve as the core carrier.Spo exhibits acid-induced contraction and alkali-induced expansion,with germinal apertures opening progressively as pH increases.In contrast,chitosan-butyrate complex(CBC)swells into a gel under acidic conditions but contracts and precipitates in alkaline environments.After drug loading into the spo,surface coating with CBC seals the germinal apertures,constructing an intelligent gate.In gastric fluid,the CBC layer gels and blocks apertures to prevent premature drug release.In intestinal fluid,CBC contracts and precipitates to open the gate;meanwhile,spo expands to further widen germinal apertures and facilitate drug release.The spiny morphology of spo,combined with the mucoadhesive properties of chitosan and active targeting of butyrate,collectively enhances intestinal adhesion and retention,enabling precise colonic drug release and accumulation.Mesalazine is formulated into liposomes to improve aqueous solubility and stability,which enhances cellular uptake and bioavailability,thereby exerting synergistic anti-inflammatory effects with butyric acid at inflamed sites.The chrysanthemum sporopollenin-based gated microcapsules exhibit favorable pH-responsive release,enhanced mucoadhesion and potent synergistic anti-inflammatory activity.This work provides a promising multifunctional targeted delivery strategy for UC therapy and establishes a novel,versatile design concept termed the opposite pH-responsive dual-gating mechanism,which supports the development of oral colon-targeted carriers capable of navigating complex gastrointestinal environments. 展开更多
关键词 Chrysanthemum sporopollenin Colon-targeted Ulcerative colitis 5-aminosalicylic acid Butyric acid Drug delivery system
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Long-term clinical outcomes with filgotinib in ulcerative colitis:12-month results from the FILGUITO study 认领 引用
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作者 Antonio M Caballero-Mateos Claudio Trigo-Salado +11 位作者 Álvaro Suárez-Toribio María del Mar Martín-Rodríguez Francisco J Rodríguez-González Teresa Valdés-Delgado Héctor Pallarés-Manrique Ana María Trapero-Martínez Raúl Olmedo-Martín Cristina Bailón-Gaona Jose Manuel Benitez Cantero B Gros Antonia Sáez-Díaz Álvaro Hernández-Martínez 《World Journal of Gastroenterology》 SCIE CAS 2026年第6期67-76,共10页
BACKGROUND Filgotinib,a JAK1-preferential inhibitor,has demonstrated efficacy in pivotal clinical trials for moderate-to-severe ulcerative colitis(UC),leading to regulatory approvals.While emerging real-world studies ... BACKGROUND Filgotinib,a JAK1-preferential inhibitor,has demonstrated efficacy in pivotal clinical trials for moderate-to-severe ulcerative colitis(UC),leading to regulatory approvals.While emerging real-world studies provide short-term effectiveness data,comprehensive long-term evidence—particularly beyond 6 months—remains scarce,especially in heavily biologic-experienced populations.AIM To evaluate the 12-month effectiveness,safety,and predictors of response to filgotinib in a real-world cohort of patients with moderate-to-severe UC treated across multiple centers in Andalusia,Spain.METHODS This multicenter,ambispective observational study(FILGUITO registry)included 104 adults with moderate-tosevere UC initiating filgotinib therapy.Demographic,clinical,laboratory,and endoscopic data were collected at baseline and at 8 weeks,6 months,and 12 months.Effectiveness outcomes included clinical remission(Mayo partial score1 and no rectal bleeding),clinical-biochemical remission(clinical remission plus fecal calprotectin<250μg/g),and steroid-free remission(clinical remission with no corticosteroid courses from week 8).Safety was assessed through adverse event monitoring.RESULTS The median age was 40.7 years(IQR:29.5-51.0),with 56.7% male patients.The majority(79.8%)had prior advanced therapy exposure,with a median of 1 prior biologic(IQR:1-3).Clinical remission rates were 60.8%at 8 weeks,61.4%at 6 months,and 60.3%at 12 months(all P<0.001 vs baseline).Clinical-biochemical remission reached 33.0%,38.6%,and 31.0%at the same timepoints.Steroid-free remission was achieved in 60.0%at 6 months and 56.9%at 12 months.Median fecal calprotectin decreased significantly from 2000μg/g at baseline(IQR:755.8-2392.5)to 153μg/g at 12 months(IQR:21.3-569.0,P<0.001).Treatment discontinuation occurred in 22.1%of patients by 12 months,primarily due to lack of response.Serious adverse events were rare(2.8%),with a favorable safety profile.Patients with only one prior biologic showed higher remission rates compared to those with multiple prior treatments.CONCLUSION Filgotinib demonstrates sustained clinical effectiveness and a favorable safety profile over 12 months in a realworld UC cohort with extensive prior biologic exposure.Effectiveness is optimized at earlier treatment lines,though meaningful benefit persists in heavily pre-treated populations. 展开更多
关键词 Filgotinib Ulcerative colitis JAK inhibitor Real-world evidence Effectiveness Safety
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Weizmannia coagulans spores alleviates DSS-induced ulcerative colitis model by modulation of gut flora,metabolites and suppressing TLR4/MyD88/NF-κB pathway 认领 引用
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作者 Ying Wu Pingping Tian +5 位作者 Junfei Li Han Gao Shanshan Tie Shumiao Zhao Huayi Suo Shaobin Gu 《Food Science and Human Wellness》 SCIE CAS CSCD 2026年第2期704-721,共18页
Ulcerative colitis(UC)is a chronic intestinal inflammatory disease characterized by a complex pathogenesis.Weizmannia coagulans has emerged as a potential probiotic for treating intestinal disorders.This study aimed t... Ulcerative colitis(UC)is a chronic intestinal inflammatory disease characterized by a complex pathogenesis.Weizmannia coagulans has emerged as a potential probiotic for treating intestinal disorders.This study aimed to assess the therapeutic impact of W.coagulans BC99 on mice with DSS-induced UC and to elucidate its underlying mechanism of action.Our findings revealed that BC99 administration ameliorated symptoms associated with DSS-induced UC mice,as evidenced by reduced disease activity indexes,reversal of weight loss,and normalization of colon length.Furthermore,BC99 treatment also protected the integrity of the intestinal barrier through maintaining the antioxidant activity and the expression of tight junction proteins(ZO-1 and occludin),and regulating the inflammatory cytokines in DSS-induced UC mice.Additionally,BC99 supplementation enhanced the production of short-chain fatty acids(SCFAs)through the proliferation of SCFA-producing bacteria,including Bidobacterium,Blautia and Faecallbaculum.Notably,the NF-κB signaling pathway was found to be closely related to BC99 treatment in DSS-induced UC mice.The positive protein expression and the m RNA expression of TLR4,My D88 and p65 in colon tissue were all detected in BC99-treated groups,which indicating that BC99 could alleviate UC symptoms by inhibiting TLR4/My D88/NF-κB signaling pathway.Metabolomics further confirms the previous results.Collectively,these findings provide basic support for the W.coagulans as a functional food additive or a promising therapeutic agent for the effective management of UC. 展开更多
关键词 Weizmannia coagulans Ulcerative colitis Intestinal barrier Gut flora Short-chain fatty acid NF-κB pathway
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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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Clostridium butyricum 11 alleviates ulcerative colitis in mice by improving intestinal microbiota and inhibiting NLRP3 inflammasome assembly mediated by JAK2/STAT3 pathway 认领 引用
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作者 Fei Wang Shujie Xu +5 位作者 Qi Wang Xiang Li Qian Jin Leijie Wang Aikun Fu Weifen Li 《Food Science and Human Wellness》 SCIE CAS CSCD 2026年第5期2207-2228,共22页
The soil is rich in microorganisms,particularly bacteria.Soil-derived Clostridium butyricum 11(CB11)had a good antibacterial effect on Clostridium perfringens,which is the main pathogenic microorganism causing necroti... The soil is rich in microorganisms,particularly bacteria.Soil-derived Clostridium butyricum 11(CB11)had a good antibacterial effect on Clostridium perfringens,which is the main pathogenic microorganism causing necrotizing enteritis in chickens.It could be deduced that CB11 may have a potential therapeutic effect on ulcerative colitis(UC).Therefore,this study aimed to evaluate the effect of CB11 on dextran sodium sulfate(DSS)-induced UC in C57BL/6 mice and its mechanism.The results showed that CB11 could significantly alleviate the pathological injury of the colon in UC mice,up-regulate the expression of colonic tight junction protein and MUC2,and decrease myeloperoxidase activity(P<0.05).Compared with the Model group,CB11 significantly increased the antioxidant capacity(total superoxide dismutase,catalase,and glutathione peroxidase)of UC mice and the related genes expression of oxidative stress(Nrf2,HO-1,and NQO1),decreased the secretion level of inflammatory factors(interleukin(IL)-1β,IL-6,IL-17A,IL-18,and tumor necrosis factor(TNF)-α),and the related genes expression of Keapl and apoptosis(Bax,Caspase 3,Caspase 8 and Caspase 9,P<0.05).Additionally,CB11 significantly reversed the intestinal microbiota imbalance caused by DSS,including Bacteroides,Culturomica,Allobaculum,Parasutterella,Helicobacter,Mucispirillum,Ligilactobacillus,Obesimuribacter,etc.Furthermore,CB 11 inhibited the activation of the JAK2/STAT3 pathway and the assembly of NLRP3 inflammasome in the colon.Fecal microbial transplantation(FMT)results verified that the intestinal microbiota regulated by CB11 markedly improved UC symptoms.These results suggested that CB11 could be utilized as a candidate probiotic to treat UC and is worthy of further research and application. 展开更多
关键词 Clostridium butyricum Ulcerative colitis Intestinal microbiota JAK2/STAT3 pathway NLRP3 inflammasome
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Sex-specific differences in the efficacy and prognosis of 5-aminosalicylic acid therapy for ulcerative colitis:A 20-year retrospective cohort study 认领 引用
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作者 Zhao-Shi Liu Hao Tang +4 位作者 Hui-Min Zhang Xiao-Yin Bai Hong Yang Xiao-Feng Li Jia-Ming Qian 《World Journal of Gastroenterology》 SCIE CAS 2026年第22期17-26,共10页
BACKGROUND Despite 5-aminosalicylic acid(5-ASA)being the first-line therapy for ulcerative colitis(UC),there is limited real-world evidence concerning sex-specific differences in the efficacy of 5-ASA therapy and pati... BACKGROUND Despite 5-aminosalicylic acid(5-ASA)being the first-line therapy for ulcerative colitis(UC),there is limited real-world evidence concerning sex-specific differences in the efficacy of 5-ASA therapy and patient prognosis.AIM To investigate sex-disparities in 5-ASA treatment responses and long-term outcomes in a Chinese large-scale UC cohort.METHODS A retrospective study was conducted on 554 consecutive UC patients treated with 5-ASA at Peking Union Medical College Hospital between January 2003 and June 2023.The rates of endoscopic mucosal healing(EMH)and colectomy were compared between the female and male cohorts,and 1:1 propensity score matching(PSM)was performed for demographics,comorbid conditions and drugs,disease conditions,laboratory parameters,and UC medication use.Cox regression analysis and Kaplan-Meier curves were constructed for survival analyses.RESULTS There were 243 patients in the female cohort(mean age,34.8±11.3 years;21.4%with ulcerative proctitis)and 311 patients in the male cohort(mean age,36.2±13.5 years;22.8%with ulcerative proctitis).After PSM,there was a higher risk of UC flare-up in the male vs female cohort[adjusted odds ratio=2.78,95%confidence interval(CI):1.69-4.55,P<0.001].Male sex was an independent protective factor against EMH[adjusted hazard ratio(aHR)=0.89,95%CI:0.87-0.91,P=0.03]and a risk factor for colectomy(aHR=1.93,95%CI:1.13-3.29,P=0.02).Male patients had longer EMH-free survival(aHR=0.63,95%CI:0.39-1.00,P=0.048)and shorter colectomy-free survival(aHR=1.80,95%CI:1.06-3.05,P=0.027).CONCLUSION Pronounced sex-specific differences exist in 5-ASA therapy efficacy and patient prognosis.Male sex is associated with more frequent relapses,a lower likelihood of EMH,and a higher risk of colectomy. 展开更多
关键词 Ulcerative colitis Inflammatory bowel disease 5-aminosalicylic acid Sex-specific differences Efficacy Prognosis Endoscopic mucosal healing Colectomy Surgery
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Agrocybe cylindracea polysaccharides repair the intestinal mucosal barrier in DSS-induced colitis by modulating the gut microbiota-macrophage axis 认领 引用
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作者 Zaoxuan Wu Shujian Wu +6 位作者 Xiuying Liu Shuze Chen Senbao Xu Yunying Gong Qiujuan Ye Xuefeng Gao Ye Chen 《Food Science and Human Wellness》 SCIE CAS CSCD 2026年第4期1702-1717,共16页
The Agrocybe cylindracea polysaccharides(ACP)have been shown to possess various health benefits.However,the anti-inflammatory effects of ACP and the mechanisms underlying these effects remain poorly understood.In this... The Agrocybe cylindracea polysaccharides(ACP)have been shown to possess various health benefits.However,the anti-inflammatory effects of ACP and the mechanisms underlying these effects remain poorly understood.In this study,we delved into the potential of ACP in mitigating colitis induced by dextrose sodium sulfate(DSS)in C57BL/6J mice and explored the associated mechanisms.ACP demonstrated notable antiinflammatory effects in the intestines,as evidenced by the restoration of various indicators such as increased body weight and colon length,decreased disease activity index(DAI)score,and alleviation of pathological damage in the colon.Additionally,ACP upregulated the expression of ZO-1,Occludin,and Muc2,suggesting a restoration of the mechanical and mucus barriers of the intestinal mucosa.Furthermore,ACP facilitated the polarization of M2 macrophages and preserved intestinal immune balance.The impact of ACP on the biological barrier was further scrutinized.ACP ameliorated disruptions in the gut microbiota,particularly by enhancing the relative abundance of bacteria that produce short-chain fatty acids(Anaerostipes,Romboutsia,and Butyricicoccus).Remarkably,the ameliorative effects of ACP on colitis were compromised upon the removal of the microbial community,but were restored post fecal microbiota transplantation(FMT),indicating that the efficacy of ACP in alleviating colitis is dependent on the gut microbiota.Intriguingly,the regulatory influence of ACP on macrophages also hinged on the gut microbiota.In essence,ACP exhibits the potential to modulate the composition of the gut microbiota,fostering the growth of beneficial bacteria,which in turn promotes the polarization of colonic M2 macrophages and facilitates the repair of the intestinal mucosal barrier in DSS-induced colitis.These findings underscore the capacity of ACP to enhance the intestinal mucosal barrier and ameliorate colitis by modulating the gut microbiota-macrophage axis,suggesting that ACP could serve as a functional food supplement for preserving intestinal homeostasis and preventing colitis. 展开更多
关键词 Agrocybe cylindracea polysaccharides Ulcerative colitis Gut microbiota M2 macrophage polarization Intestinal mucosal barrier
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Danggui-Baishao herb pair protects against dextran sulfate sodiuminduced colitis by modulating the Wnt/β-catenin pathway 认领 引用
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作者 Tian Xu Wei-Xin Hou +4 位作者 Sun-Ting Yang Yu-Pei Shao Jing Wang Tao-Tao Han Jing-Nan Li 《World Journal of Gastroenterology》 SCIE CAS 2026年第5期104-124,共21页
BACKGROUND The Danggui-Baishao herb pair is the foundation of a traditional Chinese medicine formula known as Shaoyao decoction,which is widely used in the treatment of colitis.AIM To uncover the mechanisms underlying... BACKGROUND The Danggui-Baishao herb pair is the foundation of a traditional Chinese medicine formula known as Shaoyao decoction,which is widely used in the treatment of colitis.AIM To uncover the mechanisms underlying the anti-colitis effects of the Danggui-Baishao herb pair.METHODS The chemical composition of the herb pair was characterized by high performance liquid chromatography-quadrupoleime of flight mass spectrometry analysis.A mouse model of colitis was induced by administering 2.5%dextran sulfate sodium.The therapeutic effects of the herb pair were evaluated based on body weight changes,colon length,histopathological,intestinal inflammation,and barrier function.To investigate the underlying mechanisms,RNA sequencing,metabolomics,16S rRNA sequencing,metagenomics,and theβ-catenin inhibitor ICG-001 were utilized.Furthermore,molecular docking and dextran sulfate sodiumtreated HCT 116 cells were conducted to explore the protective mechanisms of benzoylpaeoniflorin.RESULTS The herb pair improved body weight,colon length,intestinal inflammation,and barrier function.Additionally,the herb pair upregulated the expression of intestinal stem cells marker leucine-rich repeat-containing G-protein coupled receptor 5 and proliferation-related proteins.RNA sequencing analysis showed that the herb pair activated the Wnt/β-catenin signaling pathway.Metabolomic analysis revealed changes in bile acids composition.Through 16S rRNA and metagenomic sequencing,it was observed that the herb pair modulated the gut microbiota,with an enrichment of probiotics and a depletion of pathogenic bacteria.Following intraperitoneal injection of antagonist ICG-001,the therapeutic efficacy was diminished.Molecular docking showed that benzoylpaeoniflorin can bind toβ-catenin.Furthermore,benzoylpaeoniflorin can activated the Wnt/β-catenin signaling pathway and the therapeutic efficacy was also diminished by the ICG-001 in vitro.CONCLUSION The herb pair effectively reduces colonic inflammation and maintains the integrity of the intestinal barrier.Moreover,the anti-colitis efficacy of the herb pair is closely associated with activation of the Wnt/β-catenin pathway. 展开更多
关键词 Danggui-Baishao herb pair Benzoylpaeoniflorin Ulcerative colitis Wnt/β-catenin pathway Intestinal barrier Gut microbiota Bile acids
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Atractylodis Rhizoma-Atractylodis Macrocephala Rhizoma herbal pair restores intestinal mucosal barrier function in ulcerative colitis via activating Epac1/Rap1 pathway and inhibiting PI3K/AKT pathway 认领 引用
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作者 Xuecheng Yu Wenlong Su +7 位作者 Peng Huang Zengxiang Gao Yunya Lin Jiyuan Tu Yan Cao Yanju Liu Linlin Chen Guosheng Cao 《Chinese Journal of Natural Medicines》 SCIE CAS CSCD 2026年第3期313-325,共13页
Ulcerative colitis (UC) is a persistent,diffuse intestinal inflammation and ranks among the most challenging chronic diseases worldwide.Atractylodes lancea (Thunb.) DC.and Atractylodis macrocephala Koidz.are tradition... Ulcerative colitis (UC) is a persistent,diffuse intestinal inflammation and ranks among the most challenging chronic diseases worldwide.Atractylodes lancea (Thunb.) DC.and Atractylodis macrocephala Koidz.are traditional Chinese medicines (TCMs) with a long history of clinical application,particularly for gastrointestinal disorders.Both Atractylodis Rhizoma (AR)and Atractylodis Macrocephala Rhizoma (AM) have shown significant efficacy in managing UC;however,the underlying mechanism by which the AR-AM herbal pair promotes intestinal mucosal healing remains poorly understood.The therapeutic effects of the ethanolic extract of AR-AM (EEAR-AM) were evaluated in a murine UC model induced by dextran sodium sulfate(DSS).A network pharmacology approach was employed to explore the anti-UC properties of EEAR-AM,including identification of active compounds,prediction of potential targets,and construction of a protein-protein interaction (PPI) network.Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were subsequently performed to preliminarily elucidate the mechanisms of EEAR-AM in UC treatment.Finally,the proposed molecular mechanisms were validated in both DSS-induced UC mice and Caco-2 cells.In vivo results demonstrated that EEAR-AM significantly attenuated DSS-induced weight loss,reduced colon shortening,lowered the disease activity index (DAI) score,and modulated the spleen coefficient.Moreover,EEAR-AM improved colonic tissue architecture,reduced inflammatory infiltration,restored goblet cell density,enhanced mucin MUC2 expression,and elevated levels of tight junction (TJ) proteins.Additionally,EEAR-AM suppressed the expression of matrix metalloproteinase 2 (MMP-2) and MMP-9.Network pharmacology analyses indicated that EEAR-AM may ameliorate intestinal mucosal dysfunction through modulation of the exchange protein directly activated by cAMP 1 (Epac1)/Ras-associated protein 1 (Rap1) pathway and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathways.These actions potentially enhance cellular barrier integrity and reduce the release of inflammatory mediators.Western blotting results confirmed that EEAR-AM activated the Epac1/Rap1 pathway while downregulating the PI3K/AKT pathway in both DSS-induced UC mice and Caco-2cells,consistent with predictions from network pharmacology.This study represents the first evidence that the EEAR-AM herbal pair improves intestinal mucosal barrier function in UC,with therapeutic effects likely mediated by activation of the Epac1/Rap1 pathway and inhibition of the PI3K/AKT pathway. 展开更多
关键词 Ulcerative colitis Atractylodis Rhizoma-Atractylodis Macrocephala Rhizoma Epac1/Rap1 PI3K/AKT Intestinal barrier
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Rauvolfia verticillata-derived pectic polysaccharides alleviate ulcerative colitis via regulating macrophage polarization and inhibiting the JAK2/STAT3-NOS2 pathway 认领 引用
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作者 Fan Jiang Ning Liu +2 位作者 Hai-Dong Wu Xin-Pu Miao Lin Miao 《Asian Pacific Journal of Tropical Biomedicine》 SCIE CAS 2026年第4期160-172,共13页
Objective:To investigate the effect of pectic polysaccharides isolated from Rauvolfia verticillata on ulcerative colitis and its underlying mechanisms.Methods:Pectic polysaccharides were characterized using high-perfo... Objective:To investigate the effect of pectic polysaccharides isolated from Rauvolfia verticillata on ulcerative colitis and its underlying mechanisms.Methods:Pectic polysaccharides were characterized using high-performance liquid chromatography with 1-phenyl-3-methyl-5-pyrazolone pre-column derivatization,phenol-sulfuric acid assay,and gel permeation chromatography.HT-29 cells were stimulated with lipopolysaccharide and then treated with pectic polysaccharides;conditioned medium was applied to THP-1-derived macrophages to assess cell viability and polarization,while tight junction protein expression was analyzed in HT-29 cells.Furthermore,a mouse model of dextran sulfate sodium-induced colitis was treated with oral pectic polysaccharides or NOS2 overexpression.Body weight,disease activity index,colon length,histopathology,and the protein expression related to the JAK2/STAT3-NOS2 signaling were evaluated.Results:The pectic polysaccharide was characterized as an acidic pectic polysaccharide,primarily composed of galacturonic acid and various neutral sugars,with a narrow molecular weight distribution and high purity.Pectic polysaccharides significantly enhanced THP-1 macrophage viability,promoted M1 to M2 polarization,and upregulated the expression of epithelial tight junction proteins.In addition,pectic polysaccharide treatment attenuated body weight loss,lowered disease activity index scores and improved colon histology in mice with dextran sulfate sodium-induced colitis.It also reduced JAK2/STAT3 phosphorylation and NOS2 expression,and increased the expression of tight junction proteins(ZO-1,occludin,and claudin-1).Conclusions:Pectic polysaccharides attenuate ulcerative colitis by increasing M2-related macrophage markers,inhibiting the JAK2/STAT3-NOS2 signaling,and enhancing epithelial barrier-related protein expression.These findings support pectic polysaccharides as a natural candidate for the treatment of ulcerative colitis. 展开更多
关键词 Rauvolfia-derived polysaccharides Ulcerative colitis Macrophage polarization JAK2/STAT3-NOS2 signaling Epithelial barrier
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Salidroside mitigates experimental colitis through cyclic adenosine monophosphate pathway activation and suppression of enteric glial cell responses 认领 引用
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作者 Yan Li Sha-Sha Tao +4 位作者 Yan Wang Qian Sun Meng-Ying Li Hua Zhang Yun-Qing Li 《World Journal of Gastroenterology》 SCIE CAS 2026年第21期89-110,共22页
BACKGROUND Inflammatory bowel disease,particularly ulcerative colitis(UC),represents a chronic relapsing intestinal disorder of complex pathogenesis.The inflammatory cascade characteristic of UC compromises both the a... BACKGROUND Inflammatory bowel disease,particularly ulcerative colitis(UC),represents a chronic relapsing intestinal disorder of complex pathogenesis.The inflammatory cascade characteristic of UC compromises both the architecture and physiological integrity of the enteric nervous system.Salidroside(Sal),a bioactive component with well-documented anti-inflammatory and tissue-protective properties,has emerged as a potential candidate for UC treatment,yet its specific effects on enteric glial cells(EGCs)behavior and the underlying mechanisms mediating its therapeutic potential in experimental colitis remain incompletely understood.AIM To investigate how Sal regulates EGCs activation and its therapeutic pathways in experimental colitis.METHODS Colitis severity was quantified through disease activity scores,histological examination,and colonic length measurements.Mucosal barrier function was evaluated using immunofluorescent detection of tight junction proteins,ultrastructural analysis via transmission electron microscopy,and fluorescein isothiocyanate-dextran permeability assay.EGCs activation status was characterized through immunofluorescence and Western blot analysis.Systemic inflammatory markers were quantified using enzyme-linked immunosorbent assays to measure circulating cytokine concentrations.Mechanistic insights were obtained by integrating network pharmacology predictions with whole-transcriptome profiling.RESULTS Sal treatment significantly reduced disease activity index scores by(P<0.0001),preserved colon length by 11.80%compared to dextran sulfate sodium salt(DSS)group(5.23±0.16 cm vs 5.93±0.17 cm,P=0.0268),and decreased serum interleukin(IL)-1βby 78.17%[from 61.09±0.90 pg/mL to 13.33±0.68 pg/mL,P<0.0001,95%confidence interval(CI):45.10%-50.40%],IL-6 by 64.13%(from 85.96±1.73 pg/mL to 30.83±0.84 pg/mL,P<0.0001,95%CI:50.39%-59.87%),and tumor necrosis factor-αby 11.40%(from 91.06±1.92 pg/mL to 80.68±0.02 pg/mL,P=0.0054,95%CI:3.57%-17.19%)in the DSS-induced colitis model.These beneficial outcomes correlated with modulatory effects on EGCs within the enteric nervous system.Integrated network pharmacology and transcriptomic investigations revealed that Sal operates through stimulation of the cyclic adenosine monophosphate(cAMP)/protein kinase A(PKA)/cAMP-response element binding protein(CREB)cascade,which underlies its anti-colitic properties.Sal intervention suppressed EGCs reactivity across both myenteric and submucosal plexuses,evidenced by diminished glial fibrillary acidic protein expression and decreased levels of inflammatory mediators.Concurrently,Sal augmented glial cell line-derived neurotrophic factor production,reconstituted epithelial tight junction complexes,normalized intestinal permeability parameters,and promoted comprehensive restoration of mucosal barrier architecture and function.CONCLUSION Through activation of the cAMP/PKA/CREB signaling cascade,Sal suppresses pathological EGCs activation,consequently attenuating intestinal inflammatory processes,preserving mucosal barrier integrity,and ameliorating experimental colitis. 展开更多
关键词 Ulcerative colitis Cyclic adenosine monophosphate-dependent protein kinase signaling Enteric glial cells Enteric nervous system Enteric nervous network
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Gegen Qinlian decoction(葛根芩连汤)ameliorates experimental colitis in mice via ferroptosis pathway 认领 引用
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作者 HUANG Jinke ZHANG Jiaqi +3 位作者 LIU Zhihong MA Jing WANG Fengyun TANG Xudong 《Journal of Traditional Chinese Medicine》 SCIE CAS CSCD 2026年第1期34-38,共5页
OBJECTIVE:To explore whether Gegen Qinlian decoction(葛根芩连汤,GQD)targets ferroptosis pathway to ameliorate experimental colitis in mice.METHODS:A mice model of dextran sulfate sodium(DSS)induced colitis was establi... OBJECTIVE:To explore whether Gegen Qinlian decoction(葛根芩连汤,GQD)targets ferroptosis pathway to ameliorate experimental colitis in mice.METHODS:A mice model of dextran sulfate sodium(DSS)induced colitis was established and therapeutic effects of GQD were determined by detecting body weight,disease activity index(DAI),colon length and histopathological changes.Then,the expression levels of inflammatory cytokines were detected by enzyme-linked immunosorbent assay,the expression levels of tight junction proteins were detected by immunohistochemistry and the expression levels of ferroptosis-associated proteins were detected by western blotting.RESULTS:GQD treatment attenuated weight loss and DAI score,increased colon length,ameliorated intestinal histopathological damage,inhibited colonic inflammatory cytokine release and enhanced epithelial barrier function in mice with ulcerative colitis(UC).Furthermore,GQD administration obviously improved the expression of ferroptosis-associated proteins(solute carrier family 7 member 11 and acyl-Co A synthetase long chain family member 4).CONCLUSION:GQD could exert a therapeutic effect on colitis by alleviating colon damage and promoting intestinal mucosal barrier repair in DSS-induced colitis mice through the inhibition of ferroptosis,which may provide an effective natural therapy for the treatment of UC. 展开更多
关键词 colitis,ulcerative ferroptosis dextran sulfate mice Gegen Qinlian decoction
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Herbal medicine beyond probiotics:Yiyi Fuzi Baijiang powder and the holistic regulation of gut microbiota in ulcerative colitis 认领 引用
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作者 Hua-Jun Zhang Shui-Quan Jin +1 位作者 Ding-Jun Cai Zhi-Peng He 《World Journal of Gastroenterology》 SCIE CAS 2026年第1期212-215,共4页
We read with great interest the study by Zhang et al on Yiyi Fuzi Baijiang powder(YFB),which exemplifies the power of modern methods to validate traditional Chinese medicine(TCM).The key insight is that YFB doesn’t m... We read with great interest the study by Zhang et al on Yiyi Fuzi Baijiang powder(YFB),which exemplifies the power of modern methods to validate traditional Chinese medicine(TCM).The key insight is that YFB doesn’t merely alter“good”or“bad”bacteria but restores the gut microbiota’s holistic equilibrium.This is powerfully shown by its paradoxical reduction of anaerobic probiotics like Bifidobacterium,rectifying the diseased,hypoxic environment,causing their aberrant overgrowth.This challenges the conventional probiotic paradigm and underscores a core TCM principle:Herbal formulas treat disease by restoring the body’s overall functional balance.Future research should focus on the interplay between herbal components,intestinal oxygen,and microbial metabolites to further unravel this sophisticated dialogue. 展开更多
关键词 Yiyi Fuzi Baijiang powder Ulcerative colitis Gut microbiota Network pharmacology Short-chain fatty acids Multi-omics integration Nuclear factor kappa-B signaling pathway Synergistic mechanism
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