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| 1 | Relationship between intestinal microbiota and ulcerative colitis:Mechanisms and clinical application of probiotics and fecal microbiota transplantation显示文摘Ulcerative colitis(UC) is an inflammatory disease that mainly affects the colon and rectum. It is believed that genetic factors, host immune system disorders, intestinal microbiota dysbiosis, and environmental factors contribute to the pathogenesis of UC. however, studies on the role of intestinal microbiota in the pathogenesis of UC have been inconclusive. Studies have shown that probiotics improve intestinal mucosa barrier function and immune system function and promote secretion of anti-inflammatory factors, thereby inhibiting the growth of harmful bacteria in the intestine. Fecal microbiota transplantation(FMT) can reduce bowel permeability and thus the severity of disease by increasing the production of short-chain fatty acids, especially butyrate, which help maintain the integrity of the epithelial barrier. FMT can also restore immune dysbiosis by inhibiting Th1 differentiation, activity of T cells, leukocyte adhesion, and production of inflammatory factors. Probiotics and FMT are being increasingly used to treat UC, but their use is controversial because of uncertain efficacy. Here, we briefly review the role of intestinal microbiota in thepathogenesis and treatment of UC. | Zhao-hua Shen Chang-xin Zhu Yong-sheng Quan Zhen-yu Yang Shuai Wu Wei-wei Luo Bei Tan Xiao-yan Wang | 2018 | World Journal of Gastroenterology2018，24，1： | 111 |
| 2 | Inflammatory bowel disease:Pathogenesis显示文摘Inflammatory bowel disease(IBD),including Crohn’s disease and ulcerative colitis,is characterized by chronic relapsing intestinal inflammation.It has been a worldwide health-care problem with a continually increasing incidence.It is thought that IBD results from an aberrant and continuing immune response to the microbes in the gut,catalyzed by the genetic susceptibility of the individual.Although the etiology of IBD remains largely unknown,it involves a complex interaction between the genetic,environmental or microbial factors and the immune responses.Of the four components of IBD pathogenesis,most rapid progress has been made in the genetic study of gut inflammation.The latest internationally collaborative studies have ascertained 163susceptibility gene loci for IBD.The genes implicated in childhood-onset and adult-onset IBD overlap,suggesting similar genetic predispositions.However,the fact that genetic factors account for only a portion of overall disease variance indicates that microbial and environmental factors may interact with genetic elements in the pathogenesis of IBD.Meanwhile,the adaptive immune response has been classically considered to play a major role in the pathogenesis of IBD,as new studies in immunology and genetics have clarified that the innate immune response maintains the same importance in inducing gut inflammation.Recent progress in understanding IBD pathogenesis sheds lights on relevant disease mechanisms,including the innate and adaptive immunity,and the interactions between genetic factors and microbial and environmental cues.In this review,we provide an update on the major advances that have occurred in above areas. | Yi-Zhen Zhang Yong-Yu Li | 2014 | World Journal of Gastroenterology2014，20，1： | 103 |
| 3 | Moxibustion treatment modulates the gut microbiota and immune function in a dextran sulphate sodium-induced colitis rat model显示文摘AIM To investigate the effect and mechanism of moxibustion in rats with ulcerative colitis.METHODS A rat colitis model was established by administering 4% dextran sulphate sodium solution. Seventy male rats were randomly divided into seven groups: Healthy controls(HC), ulcerative colitis model group(UC), UC with 7 d of moxibustion(UC-7), UC with 14 d of moxibustion(UC-14), UC with mesalazine gavage(UC-W), HC with 7 d of moxibustion(HC-7), HC with 14 d of moxibustion(HC-14). Moxibustion was applied to the bilateral Tianshu(ST25). Gut microbiome profiling was conducted by 16 S r RNA amplicon sequencing, and PCR and ELISA determined the expression of inflammatory cytokines in colon mucosa and serum, respectively. RESULTS Moxibustion treatment restored the colonic mucosa and decreased submucosal inflammatory cell infiltration in colitis rats. Rats treated with moxibustion and mesalazine had significantly lower levels of the dominant phyla Proteobacteria and the genera Saccharibacteria, Sphingomonas and Barnesiella than colitis rats, and they could restore the microbiome to levels similar to those observed in healthy rats. UC rats had reduced alpha diversity, which could be alleviated by moxibustion therapy, and UC-7 had a higher alpha diversity than UC-14. This finding suggests that short-term(7 d) but no longer term(14 d) moxibustion treatment may significantly affect the gut microbiome. The potential bacterial functions affected by moxibustion may be ascorbate and aldarate metabolism, and amino acid metabolism. Compared with HC group, the levels of the cytokines interleukin-12(IL-12)(P < 0.05) and IL-6, IL-17, IL-23, interferon-γ, lipopolysaccharide, Ig A, tumour necrosis factor-α and its receptors 1(TNFR1) and TNFR2(P < 0.01) were all increased, whereas anti-inflammatory cytokine IL-2 and IL-10(P < 0.01) and transforming growth factor-β(P < 0.05) were decreased in UC rats. These changes were reversed by moxibustion.CONCLUSION Our findings suggest that moxibustion exerts its therapeutic effect by repairing mucosal tissue damage and modulating the gut microbiome and intestinal mucosal immunity. | Qin Qi Ya-Nan Liu Xiao-Ming Jin Lin-Shuang Zhang Cun Wang Chun-Hui Bao Hui-Rong Liu Huan-Gan Wu Xiao-Mei Wang | 2018 | World Journal of Gastroenterology2018，24，28： | 42 |
| 4 | Epidemiology, demographic characteristics and prognostic predictors of ulcerative colitis显示文摘Ulcerative colitis(UC)is a chronic disease characterized by diffuse inflammation of the mucosa of the colon and rectum.The hallmark clinical symptom of UC is bloody diarrhea.The clinical course is marked by exacerbations and remissions,which may occur spontaneously or in response to treatment changes or intercurrent illnesses.UC is most commonly diagnosed in late adolescence or early adulthood,but it can occur at any age.The incidence of UC has increased worldwide over recent decades,especially in developing nations.In contrast,during this period,therapeutic advances have improved the life expectancy of patients,and there has been a decrease in the mortality rate over time.It is important to emphasize that there is considerable variability in the phenotypic presentation of UC.Within this context,certain clinical and demographic characteristics are useful in identifying patients who tend to have more severe evolution of the disease and a poor prognosis.In this group of patients,better clinical surveillance and more intensive therapy may change the natural course of the disease.The aim of this article was to review the epidemiology and demographic characteristics of UC and the factors that may be associated with its clinical prognosis. | Bruno César da Silva Andre Castro Lyra Raquel Rocha Genoile Oliveira Santana | 2014 | World Journal of Gastroenterology2014，20，28： | 48 |
| 5 | A chronic ulcerative colitis model in rats显示文摘INTRODUCTIONIn recent years,there have been many reports aboutanimal model to investigate drugs for inflammatorybowel diseases (IBD).The experimental animalmodel often used is acetic acid-induced damage ofcolonic muscosa.In the present study,this animalmodel was investigated by administering variousconcentrations of TNBS. | Zheng L Gao ZQ Wang SX | 2000 | World Journal of Gastroenterology2000，6，1： | 37 |
| 6 | Contribution of the IL-17/IL-23 axis to the pathogenesis of inflammatory bowel disease显示文摘Inflammatory bowel diseases(IBDs) are chronic disorders of modern society, requiring management strategies aimed at prolonging an active life and establishing the exact etiology and pathogenesis.These idiopathic diseases have environmental, genetic,immunologic, inflammatory, and oxidative stress components. On the one hand, recent advances have shown that abnormal immune reactions against the microorganisms of the intestinal flora are responsible for the inflammation in genetically susceptible individuals. On the other hand, in addition to T helper cell-type(Th) 1 and Th2 immune responses,other subsets of T cells, namely regulatory T cells and Th17 maintained by IL-23 are likely to develop IBD. IL-23 acts on innate immune system members and also facilitates the expansion and maintenance of Th17 cells. The IL-17/IL-23 axis is relevant in IBD pathogenesis both in human and experimental studies. Novel biomarkers of IBD could be calprotectin,microRNAs, and serum proinflammatory cytokines.An efficient strategy for IBD therapy is represented by the combination of IL-17 A and IL-17 F in acute IL-17 A knockout TNBS-induced colitis, and also definite decrease of the inflammatory process in IL-17 F knockout, DSS-induced colitis have been observed.Studying the correlation between innate and adaptive immune systems, we hope to obtain a focused reviewin order to facilitate future approaches aimed at elucidating the immunological mechanisms that control gut inflammation. | Cristina-Sorina Cǎanǎ Ioana Berindan Neagoe Vasile Cozma Cristian Magdas Flaviu Tǎbǎan Dan Lucian Dumitrasu | 2015 | World Journal of Gastroenterology2015，21，19： | 37 |
| 7 | Tight junctions in inflammatory bowel diseases and inflammatory bowel disease associated colorectal cancer显示文摘Inflammatory bowel diseases are characterised by inflammation that compromises the integrity of the epithelial barrier. The intestinal epithelium is not only a static barrier but has evolved complex mechanisms to control and regulate bacterial interactions with the mucosal surface. Apical tight junction proteins are critical in the maintenance of epithelial barrier function and control of paracellular permeability. The characterisation of alterations in tight junction proteins as key players in epithelial barrier function in inflammatory bowel diseases is rapidly enhancing our understanding of critical mechanisms in disease pathogenesis as well as novel therapeutic opportunities. Here we give an overview of recent literature focusing on the role of tight junction proteins, in particular claudins, in inflammatory bowel diseases and inflammatory bowel disease associated colorectal cancer. | Jonathan Landy Emma Ronde Nick English Sue K Clark Ailsa L Hart Stella C Knight Paul J Ciclitira Hafid Omar Al-Hassi | 2016 | World Journal of Gastroenterology2016，22，11： | 39 |
| 8 | Implication of miRNAs for inflammatory bowel disease treatment:Systematic review显示文摘Inflammatory bowel disease(IBD)is believed to develop via a complex interaction between genetic,environmental factors and the mucosal immune system.Crohn’s disease and ulcerative colitis are two major clinical forms of IBD.MicroRNAs(miRNAs)are a class of small,endogenous,noncoding RNA molecules,and evolutionary conserved in animals and plants.It controls protein production at the post-transcriptional level by targeting mRNAs for translational repression or degradation.MiRNAs are important in many biological processes,such as signal transduction,cellular proliferation,differentiation and apoptosis.Considerable attention has been paid on the key role of miRNAs in autoimmune and inflammatory disease,especially IBD.Recent studies have identified altered miRNA profiles in ulcerative colitis,Crohn’s disease and inflammatory bowel diseaseassociated colorectal cancer.In addition,emerging data have implicated that special miRNAs which suppress functional targets play a critical role in regulating key pathogenic mechanism in IBD.MiRNAs were found involving in regulation of nuclear transcription factor kappa B pathway(e.g.,miR-146a,miR-146b,miR-122,miR-132,miR-126),intestinal epithelial barrier function(e.g.,miR-21,miR-150,miR-200b)and the autophagic activity(e.g.,miR-30c,miR-130a,miR-106b,miR-93,miR-196).This review aims at discussing recent advances in our understanding of miRNAs in IBD pathogenesis,their role as disease biomarkers,and perspective for future investigation and clinical application. | Wei-Xu Chen Li-Hua Ren Rui-Hua Shi | 2014 | World Journal of Gastrointestinal Pathophysiology2014，5，2： | 31 |
| 9 | Risk factors associated with the development of ischemic colitis显示文摘AIM:To ascertain the role of cardiovascular risk factors,cardiovascular diseases,standard treatments and other diseases in the development of ischemic colitis(IC).METHODS:A retrospective,case-control study was designed,using matched data and covering 161 incident cases of IC who required admission to our hospital from 1998 through 2003.IC was diagnosed on the basis of endoscopic findings and diagnostic or compatible his-tology.Controls were randomly chosen from a cohort of patients who were admitted in the same period and required a colonoscopy,excluding those with diagnosis of colitis.Cases were matched with controls(ratio 1:2),by age and sex.A conditional logistic regression was performed.RESULTS:A total of 483 patients(161 cases,322 con-trols)were included;mean age 75.67±10.03 years,55.9%women.The principal indications for colonos-copy in the control group were lower gastrointestinal hemorrhage(35.4%),anemia(33.9%),abdominal pain(19.9%)and diarrhea(9.6%).The endoscopic findings in this group were hemorrhoids(25.5%),diverticular disease(30.4%),polyps(19.9%)and colorectal cancer(10.2%).The following variables were associated with IC in the univariate analysis:arterial hypertension(P= 0.033);dyslipidemia(P<0.001);diabetes mellitus(P =0.025);peripheral arterial disease(P=0.004);heart failure(P=0.026);treatment with hypotensive drugs(P=0.023);angiotensin-converting enzyme inhibitors;(P=0.018);calcium channel antagonists(P=0.028);and acetylsalicylic acid(ASA)(P<0.001).Finally,the following variables were independently associated with the development of IC:diabetes mellitus[odds ratio(OR)1.76,95%confidence interval(CI):1.001-3.077,P=0.046];dyslipidemia(OR 2.12,95%CI:1.26-3.57,P=0.004);heart failure(OR 3.17,95%CI:1.31-7.68,P=0.01);peripheral arterial disease(OR 4.1,95%CI:1.32-12.72,P=0.015);treatment with digoxin(digitalis)(OR 0.27,95%CI:0.084-0.857,P=0.026);and ASA(OR 1.97,95%CI:1.16-3.36,P=0.012).CONCLUSION:The development of an episode of IC was independently associated with diabetes,dyslipid-emia,presence of heart failure,peripheral arterial dis-ease and treatment with digoxin or ASA. | Joaquín Cubiella Fernández Luisa Núez Calvo Elvira González Vázquez Maria Jesús García García Maria Teresa Alves Pérez Isabel Martínez Silva Javier Fernández Seara | 2010 | World Journal of Gastroenterology2010，16，36： | 27 |
| 10 | Morphological study on colonic pathology in ulcerative colitis treated by moxibustion显示文摘AIM To observe the therapeutic effect ofmoxibustion on ulcerative colitis and itsinfluence on the colonic mucosal morphology.METHODS Forty-six patients with ulcerativecolitis were randomly divided into themoxibustion with herbal medicine underneathgroup and the western medicine group.Thirtypatients were treated with the abovemoxibustion and 16 patients with Salicylayefapyridine(SASP).The colonic mucosa of 13patients in the moxibustion group was observedby colonoscopy before and after the treatment.Mucin was also analyzed by H.E and AB-PASstaining.RESULTS Seventeen patients were clinicallycured,12 were improved and 1 unchanged in themoxibustion group.In the control group,5patients were clinically cured,7 improved and 4unchanged.Thirteen patients with active UCwere taken as the subjects for histopathologicanalysis in this study.The colonic mucosallesions were remarkably improved and thecharacteristic of the mucin also changed.Inmost sections,the chronic inflammation ofmucosa was geatly ameliorated(P<0.01).Theinflammatory cell infiltratation much decreased and neutrophils,disapeared in most sections(P<0.001).The goblet cells significantlyincreased(P<0.001);crypt paracrypt abscessor mucosal ulceration was seen(P<0.001).CONCLUSION The rate of cure of ulcerative colitis by moxibustion with herbal medicine beneath is superior to that by SASP. This sort of moxibustion can effectively improve the colonic mucosal lesions and restore the proportion of mucoprotein to near normal. | Huan Gan Wu Li Bin Zhou Da Ren Shi Shi Min Liu Hui Rong Liu Bi Meng Zhang Han Ping Chen Lin Shan Zhang | 2000 | World Journal of Gastroenterology2000，6，6： | 28 |
| 11 | Role of moxibustion in inflammatory responses during treatment of rat ulcerative colitis显示文摘AIM: To investigate the efficacy of moxibustion in ulcerative colitis(UC) rats from morphological, immunological and molecular biological perspectives.METHODS: Thirty-two Sprague-Dawley rats were randomly assigned to a blank control group(normal rats, n = 6) and a model replication(MR) group(UC rats, n = 26). A UC model was established by 2,4,6-trinitrobenzenesulfonic acid/dextran sulfate sodium enema. Rats in the MR group were further randomly assigned to a 9-min moxibustion(9M) group(9 moxa-cone, n = 6), 6-min moxibustion(6M) group(6 moxa-cone, n = 6), 3-min moxibustion(3M) group(3 moxa-cone, n = 6), and a waiting list control(WLC) group(no moxibustion treatment, n = 6). Rats in the moxibustion treatment group were treated in 14 sessions over 28 d. Disease activity, local tissue morphology, serum level of interleukin(IL)-8 and IL-10, and expression of Toll-like receptor(TLR)9 aswell as nuclear factor(NF)-κB p65 in colonic tissue were determined by disease activity index(DAI), hematoxylin and eosin staining, electron microscopy, enzyme-linked immunosorbent assay and Western blotting, respectively.RESULTS: DAI was lowest in the 9M group and highest in the WLC group. The differences in DAI between the moxibustion treatment(3M, 6M, 9M) and no treatment groups were significant for all one-to-one comparisons(0.60 ± 0.54 vs 1.20 ± 0.44, 0.60 ± 0.54 vs 1.80 ± 0.45, 0.60 ± 0.54 vs 3.0 ± 0.45, respectively, P < 0.05). Light and electron microscopy showed that the neatness of the glandular arrangement in colonic mucosal epithelia gradually increased in the WLC, 3M, 6M to 9M groups. IL-8 level successively decreased while IL-10 level increased from the WLC to 3M, 6M and 9M groups. The differences among these groups were significant for all comparisons(105.46 ± 8.75 vs 76.61 ± 3.58, 105.46 ± 8.75 vs 69.78 ± 1.87, 105.46 ± 8.75 vs 67.41 ± 1.84, respectively, P < 0.01 for IL-8; and 30.83 ± 1.29 vs 75.64 ± 1.90, 30.83 ± 1.29 vs 80.90 ± 3.16, 30.83 ± 1.29 vs 83.46 ± 2.37, respectively, P < 0.01 for IL-10), except comparison of 6M vs 9M. Expression of TLR9 and NF-κB p65 decreased in order: highest in the WLC group and lowest in the 9M group. In addition, the differences among the WLC, 3M, 6M and 9M groups were significant for all comparisons(0.492 ± 0.026 vs 0.380 ± 0.022, 0.492 ± 0.026 vs 0.355 ± 0.005, 0.492 ± 0.026 vs 0.327 ± 0.015, respectively, P < 0.05 for TLR9; and 0.436 ± 0.041 vs 0.326 ± 0.022, 0.436 ± 0.041 vs 0.293 ± 0.006, 0.436 ± 0.041 vs 0.265 ± 0.017, respectively, P < 0.05 for NF-κB p65).CONCLUSION: Moxibustion repairs damaged colonic mucosa, suppresses serum IL-8, activates serum IL-10 level, and decreases expression of TLR-9 and NF-κB p65 in UC rats. | Yang Han Tie-Ming Ma Mao-Lin Lu Lu Ren Xian-De Ma Zeng-Hua Bai | 2014 | World Journal of Gastroenterology2014，20，32： | 27 |
| 12 | Astragalus polysaccharide attenuates rat experimental colitis by inducing regulatory T cells in intestinal Peyer's patches显示文摘AIM: To explore probable mechanism underlying the therapeutic effect of Astragalus polysaccharide(APS) against experimental colitis.METHODS: Thirty-two Sprague-Dawley rats were randomly divided into four groups. Colitis was induced with 2, 4, 6-trinitrobenzene sulfonic acid(TNBS). The rats with colitis were treated with 400 mg/kg of APS for 7 d. The therapeutic effect was evaluated by colonic weight, weight index of the colon, colonic length, and macroscopic and histological scores. The levels of regulatory T(Treg) cells in Peyer's patches were measured by flow cytometry, and cytokines in colonic tissue homogenates were analyzed using enzyme-linked immunosorbent assay. The expression of related orphan receptor-gt(ROR-gt), IL-23 and STAT-5a was measured by Western blot.RESULTS: After 7-d treatment with APS, the weight index of the colon, colonic weight, macroscopical and histological scores were decreased, while the colonic length was increased compared with the model group. The expression of interleukin(IL)-2, IL-6, IL-17, IL-23 and ROR-gt in the colonic tissues was down-regulated, but Treg cells in Peyer's patches, TGF-β and STAT5 a in the colonic tissues were up-regulated.CONCLUSION: APS effectively ameliorates TNBSinduced experimental colitis in rats, probably through restoring the number of Treg cells, and inhibiting IL-17 levels in Peyer's patches. | Hai-mei Zhao Yan Wang Xiao-Ying Huang min-fang Huang Rong Xu Hai-Yang Yue Bu-gao Zhou Hong-Yan Huang Qi-meng Sun Duan-Yong Liu | 2016 | World Journal of Gastroenterology2016，22，11： | 28 |
| 13 | Mesenchymal stem cells alleviate TNBS-induced colitis by modulating inflammatory and autoimmune responses显示文摘AIM: To investigate the potential therapeutic effects of mesenchymal stem cells (MSCs) in inflammatory bowel disease (IBD), we transplanted MSCs into an experimental model of IBD. METHODS: A rectal enema of trinitrobenzene sulfonic acid (TNBS) (100 mg/kg body weight) was administered to female BALB/c mice. Bone marrow mesenchymal stem cells (BMSCs) were derived from male green fluorescent protein (GFP) transgenic mice and were transplanted intravenously into the experimental animals after disease onset. Clinical activity scores and histological changes were evaluated. GFP and Sex determining region Y gene (SRY ) expression were used for cell tracking. Ki67 positive cells and Lgr5-expressing cells were determined to measure proliferative activity. Inflammatory response was determined by mea-suring the levels of different inflammatory mediators in the colon and serum. The inflammatory cytokines included tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), interleukin-2 (IL-2), IL-6, IL-17, IL-4, IL-10, and transforming growth factor (TGF-β). Master regulators of Th1 cells (T-box expressed in T cells, T-bet), Th17 cells (retinoid related orphan receptor gamma(t), RORγt), Th2 cells (GATA family of transcription factors 3, GATA3) and regulatory T cells (forkhead box P3, Foxp3) were also determined. RESULTS: Systemic infusion of GFP-BMSCs ameliorated the clinical and histopathologic severity of colitis, including body weight loss, diarrhea and inflammation, and increased survival (P < 0.05). The cell tracking study showed that MSCs homed to the injured colon. MSCs promoted proliferation of intestinal epithelial cells and differentiation of intestinal stem cells (P < 0.01). This therapeutic effect was mainly mediated by downregulation of both Th1-Th17-driven autoimmune and inflammatory responses (IL-2, TNF-α, IFN-γ, T-bet; IL-6, IL-17, RORγt), and by up-regulation of Th2 activities (IL-4, IL-10, GATA-3) (P < 0.05). MSCs also induced activated CD4 + CD25 + Foxp3 + regulatory T cells (TGF-β, IL-10, Foxp3) with a suppressive capacity on Th1-Th17 effecter responses and promoted Th2 differentiation in vivo (P < 0.05). CONCLUSION: MSCs are key regulators of immune and inflammatory responses and may be an attractive candidate for cell-based therapy of IBD. | Qian-Qian Chen Li Yan Chang-Zheng Wang Wei-Hua Wang Hui Shi Bin-Bin Su Qing-Huan Zeng Hai-Tao Du Jun Wan | 2013 | World Journal of Gastroenterology2013，19，29： | 25 |
| 14 | Unconjugated bilirubin alleviates experimental ulcerative colitis by regulating intestinal barrier function and immune inflammation显示文摘BACKGROUND Unconjugated bilirubin(UCB) is generally considered toxic but has gained recent prominence for its anti-inflammatory properties. However, the effects of it on the interaction between intestinal flora and organisms and how it influences immune responses remain unresolved.AIM To investigate the role of UCB in intestinal barrier function and immune inflammation in mice with dextran-sulfate-sodium-induced colitis.METHODS Acute colitis was induced by 3%(w/v) dextran sulfate sodium salt in drinking water for 6 d followed by untreated water for 2 d. Concurrently, mice with colitis were administered 0.2 mL UCB(400 μmol/L) by intra-gastric gavage for 7 d.Disease activity index(DAI) was monitored daily. Mice were sacrificed at the end of the experiment. The length of the colon and weight of the spleen were recorded. Serum level of D-lactate, intestinal digestive proteases activity, and changes to the gut flora were analyzed. In addition, colonic specimens were analyzed by histology and for expression of inflammatory markers and proteins.RESULTS Mice treated with UCB had significantly relieved severity of colitis, including lower DAI, longer colon length, and lower spleen weight(colon length: 4.92 ±0.09 cm vs 3.9 ± 0.15 cm; spleen weight: 0.33 ± 0.04 vs 0.74 ± 0.04, P < 0.001). UCB administration inactivated digestive proteases(chymotrypsin: 18.70 ± 0.69 U/g vs44.81 ± 8.60 U/g; trypsin: 1.52 ± 0.23 U/g vs 9.05 ± 1.77 U/g, P < 0.01), increased expression of tight junction(0.99 ± 0.05 vs 0.57 ± 0.03, P < 0.001), decreased serum level of D-lactate(31.76 ± 3.37 μmol/L vs 54.25 ± 1.45 μmol/L, P < 0.001), and lowered histopathological score(4 ± 0.57 vs 7 ± 0.57, P < 0.001) and activity of myeloperoxidase(46.79 ± 2.57 U/g vs 110.32 ± 19.19 U/g, P < 0.001). UCB also regulated the intestinal microbiota, inhibited expression of tumor necrosis factor(TNF) α and interleukin 1β(TNF-α: 52.61 ± 7.81 pg/mg vs 105.04 ± 11.92 pg/mg,interleukin 1β: 13.43 ± 1.68 vs 32.41 ± 4.62 pg/mg, P < 0.001), decreased expression of Toll-like receptor 4(0.61 ± 0.09 vs 1.07 ± 0.03, P < 0.001) and myeloid differentiation primary response gene 88(0.73 ± 0.08 vs 1.01 ± 0.07, P <0.05), and increased expression of TNF-receptor-associated factor 6(0.79 ± 0.02 vs0.43 ± 0.09 P < 0.05) and inhibitor of kappa B α(0.93 ± 0.07 vs 0.72 ± 0.07, P < 0.05)in the colon.CONCLUSION UCB can protect intestinal barrier function, regulate normal intestinal homeostasis, and suppress inflammation via the Toll-like receptor 4/nuclear factor-κB signaling pathway. | Jia-Dong Zheng Yan He Heng-Yuan Yu Yuan-Li Liu Yi-Xuan Ge Xue-Ting Li Xue Li Yan Wang Meng-Ru Guo Yi-Lin Qu Xiao-Fa Qin Ming-Shan Jiang Xiu-Hong Wang | 2019 | World Journal of Gastroenterology2019，25，15： | 26 |
| 15 | Treatment of corticosteroid-resistant ulcerative colitis with oral low molecular weight heparin显示文摘 | Cui HF Jiang XL | 1999 | World Journal of Gastroenterology1999，5，5： | 24 |
| 16 | Multicenter case-control study of the risk factors for ulcerative colitis in China显示文摘AIM:To evaluate potential risk factors in the development of ulcerative colitis(UC) in China.METHODS:A total of 1308 patients with UC and 1308 age-matched and sex-matched controls were prospectively studied in China.The UC cases were collected from 17 hospitals in China from April 2007 to April 2010.Uniform questionnaires were designed to investigate risk factors including smoking,appendectomy,stress,socio-economic conditions,nonsteroidal antiinflammatory drugs(NSAIDs),oral contraceptives,diet,breastfeeding,infections and family sanitary conditions.Group comparisons by each factor were done using simple logistic regression analysis.Conditional logistic regression was used for multivariate analysis.RESULTS:By univariate analysis,the variables predictive of UC included feeling stress,light and heavy alcoholic drinking,spicy food,sugar consumption and infectious diarrhea,while heavy tea intake and tap water consumption were protective against UC.On multivariate analysis,the protective factor for UC was tap water consumption [odds ratios(OR) = 0.424,95%CI:0.302-0.594,P < 0.001];while the potential risk factors for UC were heavy sugar consumption(OR = 1.632,95%CI:1.156-2.305,P < 0.001),spicy food(light intake:OR = 3.329,95%CI:2.282-4.857,P < 0.001;heavy intake:OR = 3.979,95%CI:2.700-5.863,P < 0.001),and often feeling stress(OR = 1.981,95%CI:1.447-2.711,P < 0.001).Other factors,such as smoking habit,appendectomy,breastfeeding,a history of measles,rural or urban residence,education,oral contraceptives,and NSAID use have not been found to have a significant association with the development of UC in the present study.CONCLUSION:Our study showed tap water consumption was a protective factor for UC,while spicy food,heavy sugar consumption and often feeling stress were risk factors for UC in this Chinese population. | Yu-Fang Wang Qin Ou-yang Bing Xia Li-Na Liu Fang Gu Kai-Fang Zhou Qiao Mei Rui-Hua Shi Zhi-Hua Ran Xiao-Di Wang Pin-Jin Hu Kai-Chun Wu Xin-Guang Liu Ying-Lei Miao Ying Han Xiao-Ping Wu Guo-Bing He Jie Zhong Guan-Jian Liu | 2013 | World Journal of Gastroenterology2013，19，11： | 24 |
| 17 | Effect of resveratrol on Treg/Th17 signaling and ulcerative colitis treatment in mice显示文摘AIM:To determine the therapeutic efficacy of resveratrol on ulcerative colitis(UC) and its underlying mechanisms.METHODS:The mouse UC model was developed using 5% dextran sulfate sodium.Mice were randomly divided into four groups:normal control,UC model group,resveratrol low-dose group(RLD; 50 mg/kg per day),and resveratrol high-dose group(RHD; 100 mg/kg per day).RESULTS:The results showed that RLD regulates Treg/Th17 balance mainly through reducing the number of Th17 cells,whereas RHD regulates Treg/Th17 balance through both downregulating the number of Th17 cells and upregulating the number of Treg cells.Resveratrol can also regulate the level of plasma and intestinal mucosal cytokines including interleukin(IL)-10,transforming growth factor-β1,IL-6,and IL-17.The expressions of hypoxia inducible factor(HIF)-1α,mammalian target of rapamycin(m TOR),and signal transducer and activator of transcription 3 weresignificantly decreased in the intestinal tissues of mice treated with resveratrol.CONCLUSION:The therapeutic efficacy of resveratrol in UC is dose dependent and closely associated with the regulation of Treg/Th17 balance and the HIF-1α/mT OR signaling pathway. | Jun Yao Cheng Wei Jian-Yao Wang Ru Zhang Ying-Xue Li Li-Sheng Wang | 2015 | World Journal of Gastroenterology2015，21，21： | 23 |
| 18 | Diet therapy for inflammatory bowel diseases: The established and the new显示文摘Although patients with inflammatory bowel diseases(IBD) have a strong interest in dietary modifications as part of their therapeutic management, dietary advice plays only a minor part in published guidelines. The scientific literature shows that dietary factors might influence the risk of developing IBD, that dysbiosis induced by nutrition contributes to the pathogenesis of IBD, and that diet may serve as a symptomatic treatment for irritable bowel syndrome-like symptoms in IBD. The role of nutrition in IBD is underscored by the effect of various dietary therapies. In paediatric patients with Crohn's disease(CD) enteral nutrition(EN) reaches remission rates similar to steroids. In adult patients, however, EN is inferior to corticosteroids. EN is not effective in ulcerative colitis(UC). Total parenteral nutrition in IBD is not superior to steroids or EN. The use of specific probiotics in patients with IBD can be recommended only in special clinical situations. There is no evidence for efficacy of probiotics in CD. By contrast, studies in UC have shown a beneficial effect in selected patients. For patients with pouchitis, antibiotic treatment followed by probiotics, like VSL#3 or Lactobacillus GG, is effective. When probiotics are used, the risk of bacterial translocation and subsequent bacteremia has to be considered. More understanding of the normal intestinal microflora, and better characterization of probiotic strains at the phenotypic and genomic levels is needed as well as clarification of the mechanisms of action in different clinical settings. A FODMAP reduced diet may improve symptoms in IBD. | Franziska Durchschein Wolfgang Petritsch Heinz F Hammer | 2016 | World Journal of Gastroenterology2016，22，7： | 22 |
| 19 | Endoscopy in inflammatory bowel disease: Role in diagnosis, management, and treatment显示文摘Endoscopy plays a fundamental role in the diagnosis, management, and treatment of inflammatory bowel dis-ease(IBD). Colonoscopy, flexible sigmoidoscopy, and esophagogastroduodenoscopy have long been used in the care of patients with IBD. As endoscopic technologies have progressed, tools such as endoscopic ultrasound, capsule endoscopy, and balloon-assisted enteroscopy have expanded the role of endoscopy in IBD. Furthermore, chromoendoscopy has enhanced our ability to detect dys-plasia in IBD. In this review article, we will focus on the roles, indications, and limitations of these tools in IBD. We will also discuss the most commonly used endoscopic scoring systems, as well as special considerations in post-surgical patients. Lastly, we will discuss the role of endoscopy in the diagnosis and management of fistulae and strictures. | Clayton M Spiceland Nilesh Lodhia | 2018 | World Journal of Gastroenterology2018，24，35： | 23 |
| 20 | Colorectal cancer surveillance in inflammatory bowel disease:Practice guidelines and recent developments显示文摘Patients with long-standing inflammatory bowel disease(IBD)involving at least 1/3 of the colon are at increased risk for colorectal cancer(CRC).Advancements in CRC screening and surveillance and improved treatment of IBD has reduced CRC incidence in patients with ulcerative colitis and Crohn’s colitis.Most cases of CRC are thought to arise from dysplasia,and recent evidence suggests that the majority of dysplastic lesions in patients with IBD are visible,in part thanks to advancements in high definition colonoscopy and chromoendoscopy.Recent practice guidelines have supported the use of chromoendoscopy with targeted biopsies of visible lesions rather than traditional random biopsies.Endoscopists are encouraged to endoscopically resect visible dysplasia and only recommend surgery when a complete resection is not possible.New technologies such as virtual chromoendoscopy are emerging as potential tools in CRC screening.Patients with IBD at increased risk for developing CRC should undergo surveillance colonoscopy using new approaches and techniques. | William T Clarke Joseph D Feuerstein | 2019 | World Journal of Gastroenterology2019，25，30： | 23 |
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