Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Colitis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,135 records · Page 63Linked to original sources
PubMed2003

Serotonin availability is increased in mucosa of guinea pigs with TNBS-induced colitis.

5-HT released from enterochromaffin cells acts on enteric nerves to initiate motor reflexes. 5-HT's actions are terminated by a serotonin reuptake transporter (SERT). In this study, we tested the hypothesis that inflammation leads to altered mucosal 5-HT signaling. Colitis was induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS), and experiments were conducted on day 6. 5-HT content, number of 5-HT-immunoreactive cells, and the proportion of epithelial cells that were 5-HT-immunoreactive increased twofold in colitis. The amount of 5-HT released under basal and stimulated conditions was significantly increased in colitis. SERT inhibition increased the 5-HT concentration in media bathing-stimulated control tissue to a level comparable to that of the stimulated colitis tissue. mRNA encoding SERT and SERT immunoreactivity were reduced during inflammation. Slower propulsion and reduced sensitivity to 5-HT-receptor antagonism were observed in colitis. These data suggest that colitis alters 5-HT signaling by increasing 5-HT availability while decreasing 5-HT reuptake. Altered 5-HT availability may contribute to the dysmotility of inflammatory bowel disease, possibly due to desensitization of 5-HT receptors.

Animals↗
PubMed1997

Stress-induced enhancement of colitis in rats: CRF and arginine vasopressin are not involved.

Because exacerbation of colitis seems to be associated with stress, we proposed evaluating the influence of stress and the involvement of corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) on experimental colitis in rats. Partial restraint stress was applied during 4 consecutive days, before or after intracolonic 2,4,6-trinitrobenzenesulfonic acid (TNB) instillation (15 mg) in rats. Finally, two groups of rats were centrally injected with alpha-helical CRF-(9-41) (5 micrograms) or AVP antagonist (5 micrograms) before each session of stress. Stress was applied before or right after TNB enhanced colitis, with an increase in macroscopic and histological scores and myeloperoxidase activity, alpha-Helical CRF-(9-41) or AVP antagonist had no effect on TNB-induced colitis but enhanced the effects of stress on colitis. These results show that stress may exacerbate experimental colitis in rats and that CRF and AVP are not responsible for this effect.

Animals↗
PubMed1999

Susceptibility of Lewis and Fischer rats to stress-induced worsening of TNB-colitis: protective role of brain CRF.

We assessed the role of central corticotropin-releasing factor (CRF) in stress-induced worsening of colitis in inbred rat strains with hypo (Lewis/N) and hyper (Fischer344/N) CRF responses to stress. Intracolonic administration of 2,4,6-trinitrobenzenesulfonic acid (TNB) induced colitis of similar severity in both strains as assessed on day 7 by macroscopic scoring, histological evaluation, tissue myeloperoxidase (MPO) activity, and decrease in food intake and body weight. Colitis was inhibited by daily intracerebroventricular injections of CRF in both strains. Chronic stress (3 h/day, water avoidance or wrap restraint on alternate days for 6 days) aggravated colitis more in Lewis than Fischer rats (71 and 22% further increase in MPO activity, respectively). The CRF antagonist astressin injected intracerebroventricularly enhanced the colitis response to stress and caused mortality in both strains. Fischer rats had higher plasma corticosterone levels 20 min after stress alone on day 1 and after TNB plus stress on days 1 and 3 compared with Lewis. These data show that central CRF restrains the proinflammatory action of stress in experimental colitis.

Animals↗
PubMed2002

HPA-axis responses during experimental colitis in the rat.

We investigated the responses of the hypothalamic-pituitary-adrenal (HPA) axis during experimental colitis induced by intracolonic administration of 2,4,6-trinitrobenzenesulfonic acid in the rat. On days 3 and 7 after induction of colitis, the corticotropin-releasing hormone (CRH) mRNA level in the parvocellular paraventricular nucleus (pPVN) of the hypothalamus was reduced, the plasma ACTH level remained at the basal level, and the plasma corticosterone (Cort) level was high. Induction of colitis on day 3 after adrenalectomy with Cort pellet replacement (ADX + Cort) resulted in a marked increase in CRH mRNA on day 7 after induction of colitis compared with noncolitic ADX + Cort animals. Pair feeding to match the food intake of the colitic animals resulted in no significant change in CRH mRNA in the pPVN, plasma ACTH, and Cort compared with healthy control animals. These findings indicated that CRH mRNA expression in the pPVN was inhibited by glucocorticoid feedback during this experimental colitis, and the decrease in food intake during colitis was not simply responsible for the expression of CRH mRNA. It is inferred that the HPA axis including the CRH level in the pPVN is altered in patients with inflammatory bowel disease.

Adrenalectomy↗
PubMed1993

On the suppression of food intake in experimental models of colitis in the rat.

We measured daily food intake and body weight in rats before and after the induction of colitis by intrarectal administration of either 2,4,6-trinitrobenzenesulfonic acid in ethyl alcohol (TNBE) or 4% acetic acid (AA). Administration of TNBE or AA induced inflammation in the distal colon, which was reflected by a significant increase in myeloperoxidase (MPO) activity in the colon. On days 1, 2, and 3 after induction of colitis by TNBE, food intake fell by 80, 70, and 50%, respectively, compared with pretreatment values; food intake returned to normal by day 4. Body weight fell within 24 h after induction of colitis and remained 10% less than control for at least 5 days. Colitis induced by AA produced a similar pattern and degree of decreased food intake and weight loss. Treatment with the 5'-lipoxygenase inhibitor MK-886 significantly reduced concentrations of leukotriene B4 in the colon of TNBE-treated rats but did not affect food intake. In contrast, the cyclooxygenase inhibitor indomethacin decreased prostaglandin E2 concentrations in the colon but also attenuated the suppression of feeding by 52 and 64% on the first 2 days after induction of colitis by TNBE. These results identify a specific prostaglandin-mediated suppression of feeding in the rat with acute colitis induced by TNBE and illustrate the utility of this model for studying mechanisms underlying anorexia associated with inflammation of the gastrointestinal tract.

Acetates↗
PubMed2003

Ischemic colitis after weight-loss medication.

BACKGROUND: Previous weight-loss medications have received cautious support due to their association with pulmonary hypertension and valvular heart disease. However, newer drugs are increasingly being recommended as potentially safer and more efficacious. We report a case of ischemic colitis possibly linked to the use of a weight-loss drug, and review the literature to highlight an important latent consequence of these medications. CASE REPORT: A 59-year-old obese woman presented to the emergency room with rectal bleeding and suprapubic abdominal pain. Her medical history was unremarkable for risk factors for bowel ischemia. An appetite suppressant, phentermine 15 mg daily, had been prescribed, and had resulted in a 12 kg weight loss over 10 weeks. Colonoscopy and biopsies both demonstrated findings typical of mild ischemia at the splenic flexure. DISCUSSION: Phentermine, an amphetamine-derived sympathomimetic, acts centrally to suppress appetite. While there are no published reports linking the use of phentermine as a single agent to ischemic colitis, phentermine alone has been associated with ischemic neurological events and, when used in combination with fenfluramine, has been implicated in a single case of acute ischemic colitis. Other sympathomimetics, such as cocaine, have been clearly linked with ischemic colitis. CONCLUSIONS: This report describes a temporal association with the use of phentermine and the development of ischemic colitis. Heightened awareness and appropriate surveillance is warranted to determine whether the use of weight-loss drugs, such as phentermine, can lead to ischemic colitis.

Appetite Depressants↗
PubMed2003

Octreotide treatment of massive hemorrhage due to cytomegalovirus colitis.

Cytomegalovirus (CMV)-associated colitis can result in abdominal pain, diarrhea, significant blood loss and perforation. The standard therapy for CMV colitis includes supportive measures and antiviral medications. Severe hemorrhage due to CMV colitis often necessitates surgical resection. We present a case of a patient who was undergoing chemotherapy for acute B-cell lymphoblastic leukemia and developed significant abdominal pain and diarrhea followed by massive hematochezia. Colonoscopy showed numerous actively bleeding deep ulcers in the cecum. A provisional diagnosis of CMV colitis was made and she was started on ganciclovir. Histological assessment confirmed the diagnosis of CMV colitis. She continued to bleed profusely per rectum over the following five days, passing up to 1 L to 1.5 L of blood per day. She required 10 units of packed red blood cells over this time period. The patient refused surgical intervention and after discussion of possible options, octreotide was instituted. Her blood loss stopped almost immediately and she required no further transfusions. She tolerated the medication well and was discharged home at a later date in stable condition. This is the first reported case of the use of octreotide in the treatment of massive hematochezia from CMV colitis.

Colitis↗
PubMed2005

[Cecal cytomegalovirus infection following appendicectomy in a patient with ulcerative colitis].

We report a patient who, 3 months after being diagnosed with ulcerative colitis, was admitted to hospital because of malaise and right lower abdominal pain. An open appendectomy was performed. Histological study showed ulcerative colitis affecting the appendix. After surgery, the patient presented a refractory outbreak of ulcerative colitis requiring treatment with steroids and cyclosporin A. Despite this treatment, the patient continued to pass abundant fresh blood associated with severe anemia. Colonoscopy showed only granular and congestive cecal mucosa. Biopsies showed intracytoplasmic inclusion bodies with immunohistochemical stains positive for cytomegalovirus (CMV) infection. Rectorrhagia and anemia quickly disappeared after beginning treatment with ganciclovir. Appendicular ulcerative colitis is not uncommonly associated with distal colitis. In addition, diffuse CMV infection complicating ulcerative colitis treatment is not unusual. By contrast, isolated, segmentary infection by CMV in the proximal colon is extremely rare. Until now, only three patients with localized CMV infection have been described, and all three cases occurred in the context of ileoanal anastomosis.

Adult↗
PubMed1999

Validation of the spanish version of the inflammatory bowel disease questionnaire on ulcerative colitis and Crohn's disease.

The objective of this study is to validate the Spanish translation of the Inflammatory Bowel Disease Questionnaire (SIBDQ) on ulcerative colitis and Crohn's disease by assessing its convergence validity, discriminatory power, reliability and sensitivity to change. For that purpose, 211 patients with inflammatory bowel disease (116 with ulcerative colitis and 95 with Crohn's disease) completed the SIBDQ, the Psychological General Well-Being Index and the EuroQol. SIBDQ was repeated in those patients who remained in stable remission and in those with changes in clinical activity. Clinical activity was assessed by the Rachmilewitz and Harvey-Bradshaw indices. Correlations among scores of SIBDQ, EuroQol, Psychological General Well-Being Index and clinical indices of activity were all positive and comparable for both diseases (r = -0. 50 to r = -0.70, p < 0.01). Analysis of variance showed that SIBDQ discriminates between different clinical degrees of activity. Cronbach's alpha was 0.96 in ulcerative colitis and Crohn's disease. SIBDQ was also highly reliable when it was repeated in clinically stable patients with ulcerative colitis (intraclass correlation coefficient = 0.82) and Crohn's disease (intraclass correlation coefficient = 0.86). SIBDQ was sensitive to clinical changes in ulcerative colitis and in Crohn's disease, whether patients entered remission (effect size -1.88 and -1.81, respectively) or relapsed (effect size 1.70 and 8.04, respectively). In conclusion, the Spanish version of the IBDQ has proven to be a valid, reliable and sensitive instrument to detect clinical changes in patients with ulcerative colitis and Crohn's disease.

Adolescent↗
PubMed2000

Significant increase in prostaglandin E-main urinary metabolite by laxative administration: comparison with ulcerative colitis.

OBJECTIVE: To assess the production of prostaglandin E(2), an important chemical mediator in diarrhea induced by laxative administration, a prostaglandin E-main urinary metabolite (7alpha-hydroxy-5,11-diketotetranor-prosta-1,16-dioic acid, PGE-MUM) was measured in healthy volunteers and compared with the values of patients with ulcerative colitis. METHODS: PGE-MUM was determined by a simplified immunoassay of bicyclic PGE-MUM and analyzed for the influence of laxative administration and active/remission phases of ulcerative colitis. RESULTS: Administration of laxatives induced a significant increase in PGE-MUM in healthy volunteers. A significant elevation was also found in the active as compared with the remission phase of ulcerative colitis. The PGE-MUM levels were significantly correlated with our modified Talstad scores, clinical disease activity indices in ulcerative colitis. It was confirmed by time course studies of individual patients that changes in PGE-MUM correlated well with colitis activity. CONCLUSION: Laxative administration induces production of prostaglandin E(2) as one of the chemical mediators, although its production grade is relatively low as compared with ulcerative colitis in the active phase.

Aged↗
PubMedDate not supplied

Role of commensal bacteria in chronic experimental colitis: lessons from the HLA-B27 transgenic rat.

Rats on Lewis or Fischer background, transgenic for human HLA-B27 and beta(2)-microglobulin genes spontaneously develop colitis, gastritis, arthritis, dermatitis, orchitis, epididymitis, carditis, alopecia and nail changes. Disease susceptibility correlates with the gene copy number and is influenced by the genetic background. The pathomechanism in this model is still not completely understood. Cell transfer experiments indicate an essential role of HLA-B27 expression in bone marrow-derived cells. On Fischer background the onset of colitis occurs at 2 months of age, peaks at 3 months of age, and plateaus. Histologic findings include inflammatory cell infiltration, mostly limited to the mucosa, crypt hyperplasia, reduction of goblet cells, occasionally crypt abscesses and early ulcers. There is evidence that normal luminal bacteria play an essential role in initiating and perpetuating chronic colitis and gastritis in HLA-B27 transgenic rats: Transgenic rats raised under germ-free conditions do not develop gastrointestinal disease, whereas transgenic littermates exposed to specific pathogen-free bacteria develop colitis and gastritis within 2-4 weeks. Obligate anaerobic bacteria, especially Bacteroides spp., may play a predominant role since metronidazole prevents colitis and transgenic germ-free rats contaminated with a cocktail of six obligate and facultative anaerobic bacteria develop colitis and gastritis only in the presence of Bacteroides vulgatus. Luminal bacteria may also be involved in trafficking and homing of inflammatory cells into remote organs, since varying cecal bacterial composition does not only alter local inflammation but also influences gastritis. Lymphocyte transfer experiments indicate a specific response to luminal bacteria. In summary, this animal model is suitable for investigating the influence of normal luminal bacteria on the cellular immune mechanism in chronic intestinal inflammation.

Animals↗
PubMed2003

Ulcerative colitis in Kuwait: a review of 90 cases.

BACKGROUND: Chronic ulcerative colitis is a disease of unknown etiology. Its incidence is on the rise in various developing countries as has been reported in studies from South-East Asia and the Middle East. There seems to be significant differences in the pattern and the clinical course of this disease in our patient population. The aim of our study is to assess the incidence and the clinical course of the disease in Kuwait. METHODS: This is a retrospective study of cases identified over a period of 14 years (1985-1999). Three hundred forty-six patients were identified to have chronic ulcerative colitis. Ninety patients were interviewed for this study. RESULTS: Chronic ulcerative colitis is being identified with increasing frequency. Our local incidence was 2.8 per 100,000 persons per year. The disease was seen in both sexes with equal frequency. It peaks at the third decade of life, with no second peak observed in the sixth decade. The disease was of mild to moderate severity in 93% of the cases. The distribution of the disease in the colon showed pancolitis in 45%, left-sided colitis in 14%, proctosigmoiditis in 21% and proctitis in 20%. Arthritis and arthralgia were the most frequent extraintestinal manifestation seen in 31%. Perianal disease, although rare in ulcerative colitis, was seen in 8%. Of interest is the fact that over 14 years of follow-up, none of our patients developed high-grade dysplasia or colorectal cancer. Four patients required total colectomy mainly due to failure of medical therapy. CONCLUSIONS: Chronic ulcerative colitis is occurring with increasing frequency similar to that seen in Western countries. The disease observed in our patient population was of mild to moderate severity, with fewer complications than reported in Western countries. It peaks in the third decade with no second peak. None of our patients developed high-grade dysplasia or colorectal carcinoma.

Adolescent↗
PubMed1994

Antibodies to neutrophil cytoplasm in Italian patients with ulcerative colitis: sensitivity, specificity and recognition of putative antigens.

We studied the prevalence of perinuclear antineutrophil cytoplasmic antibody (p-ANCA), as detected by immunofluorescence, in 290 Italian subjects. One hundred and two were affected by ulcerative colitis, 48 by Crohn's disease, 40 by gluten-sensitive enteropathy and 100 were normal subjects. The prevalence of p-ANCA was significantly higher in ulcerative colitis patients (45.1%) as compared to Crohn's disease patients (4.8%), gluten-sensitive enteropathy (0%) and normal subjects (1%; p < 0.0001 ulcerative colitis vs. all other groups). In this setting, the overall specificity of the test was 98.1% with a sensitivity of 45.1%. The specificity slightly decreased to 95.1% when ulcerative colitis patients were compared to patients with Crohn's colitis. In our series, p-ANCA appeared to be more prevalent in ulcerative colitis patients with more aggressive disease. ELISA experiments performed in order to identify the putative antigen(s) recognized by p-ANCA-positive sera showed that 8 of 12 sera positive at immunofluorescence reacted with at least one of the neutrophil preparations tested. The reactivities were directed towards various neutrophil preparations. Preabsorption with the specific antigen recognized by ELISA significantly inhibited the p-ANCA immunofluorescence reactivity indicating that p-ANCA reactivity might derive from the recognition of heterogeneous neutrophil-associated antigens.

Adolescent↗
PubMed1995

Increased rate of sialylation of colonic mucin by cultured ulcerative colitis mucosal explants.

Sialylation of mucus glycoproteins confers charge and increased resistance to enzymatic degradation. The hypothesis that mucus sialylation might be altered in ulcerative colitis has been studied using in vitro culture of mucosal biopsies for 24 h with 3H N-acetyl mannosamine as a specific sialic acid precursor. Rectal biopsies were obtained at colonoscopy from patients with clinically inactive ulcerative colitis (n = 9) and controls (n = 12) who were patients found to have a normal colonoscopy performed for iron deficiency anaemia or altered bowel habit. The incorporation of 3H N-acetyl mannosamine into mucin was increased in ulcerative colitis (n = 9; 150; 113.3-393.2 dpm/micrograms mucin, median and interquartile ranges), compared with controls (n = 12; 33.6; 19.7-68.4 dpm/micrograms; p < 0.01). The ratio of incorporation into mucin of 3H N-acetyl mannosamine/14C N-acetyl galactosamine was also increased in ulcerative colitis (3.27; 1.93-4.98 dpm/dpm), compared with controls (1.35; 1.24-1.7 dpm/dpm; p < 0.001) suggesting that the increased incorporation of N-acetyl mannosamine probably reflects an increase in the average extent of sialylation per mucin oligosaccharide chain rather than an increase in the number of oligosaccharide chains. This increase in mucin sialylation seems unlikely to have a pathogenic role in the development of colitis but provides further evidence for the similarity between the alterations that occur in ulcerative colitis, colonic polyposis and malignancy.

Acetylgalactosamine↗
PubMed2004

Microscopic colitis with giant cells: a rare new histopathologic subtype?

Collagenous and lymphocytic colitis might be part of the same disease spectrum. In this report, we present a histopathologic subtype of microscopic colitis characterized by the presence of subepithelial multinucleated giant cells. This reaction is very unusual and not explicable by any underlying disease process or previous treatment. Among 490 cases of microscopic colitis (MC) diagnosed between 1992 and 2002, we found 2 cases with macrophages and giant cells (0.4%). One case of lymphocytic colitis (LC) and 1 case of collagenous colitis (CC) presented aggregates of macrophages and giant cells located in the superficial part of the lamina propria. Infectious or non-infectious colonic granulomatous diseases were excluded on histologic, clinical, and biological grounds. The recognition of this feature in an MC is important to avoid the diagnosis of granulomatous infectious or idiopathic colitis such as Crohn's disease. Even if very unusual, this subtype of MC evolves favorably since the 2 patients responded well to corticosteroid treatment.

Aged↗
PubMed1999

Successful treatment of cytomegalovirus colitis with ganciclovir in a patient with adult T cell leukemia lymphoma: case report.

An 84-year-old patient with adult T cell leukemia lymphoma (ATLL) developed diarrhea on day 5 of chemotherapy and was diagnosed with cytomegalovirus (CMV) colitis. Sigmoidoscopy revealed multiple superficial erosions surrounded by a flare. Computed tomography (CT) and ultrasonogram of the abdomen revealed marked thickening of the colonic mucosa. There were 186 CMV antigen-positive leukocytes per 31,000 white blood cells (WBC). A colonic biopsy specimen showed typical CMV nuclear inclusions. Immunohistological study of the specimen was positive for CMV antigen. Administration of ganciclovir (DHPG) 500 mg/day for 14 days improved the diarrhea and other symptoms. On day 30 of the chemotherapy, the patient developed diarrhea again but was diagnosed with pseudomembranous colitis instead of CMV colitis. At that time, CMV antigenemia and a histologic study for CMV were negative. The stool was positive for Clostridium difficile toxin antigen. ATLL patients are believed to be immunocompromised hosts and often develop opportunistic infections such as CMV infection. Most suffer from CMV pneumonia at the end of their course of therapy. Few gastrointestinal (GI) CMV infections are seen in ATLL patients and details of CMV colitis have never been reported. When an ATLL patient develops diarrhea that barely responds to conventional therapy, CMV colitis and pseudomembranous colitis should be listed in the differential diagnosis.

Aged↗
PubMed2004

An unusual case of an ulcerative colitis flare resulting in disseminated intravascular coagulopathy and a bladder hematoma: a case report.

BACKGROUND: Disorders of coagulation have long been associated with inflammatory bowel disease. Children, as well as adults, with both active and inactive ulcerative colitis have been found to have abnormal coagulation and fibrinolysis. Disseminated intravascular coagulation arises from an overwhelming of the haemostatic regulatory mechanisms leading to an excessive generation of thrombin and a failure of the normal inhibitory pathways to prevent systemic effects of this enzyme. Ulcerative colitis has been associated with disseminated intravascular coagulation in conjunction with septicemia, toxic megacolon and surgery. CASE PRESENTATION: A fourteen-year-old boy with a history of poorly controlled ulcerative colitis presented with nonbilious emesis, hematochezia, and hematuria. Laboratory workup revealed disseminated intravascular coagulation. He was placed on triple antibiotics therapy. An infectious workup came back negative. A computerized tomography (CT) scan of the abdomen revealed a marked thickening and irregularity of the bladder wall as well as wall thickening of the rectosigmoid, ascending, transverse, and descending colon. Patient's clinical status remained stable despite a worsening of laboratory values associated with disseminated intravascular coagulation. Patient was begun on high dose intravenous steroids with improvement of the disseminated intravascular coagulation laboratory values within 12 hours and resolution of disseminated intravascular coagulopathy within 4 days. A thorough infectious workup revealed no other causes to his disseminated intravascular coagulation. CONCLUSIONS: The spectrum of hypercoagulable states associated with ulcerative colitis varies from mild to severe. Although disseminated intravascular coagulation associated with ulcerative colitis is usually related to septicemia, toxic megacolon or surgery, we present a case of an ulcerative colitis flare resulting in disseminated intravascular coagulation and a bladder hematoma.

Adolescent↗
PubMed2004

Superoxide dismutase ameliorates TNBS-induced colitis by reducing oxidative stress, adhesion molecule expression, and leukocyte recruitment into the inflamed intestine.

Oxidant stress has been implicated in the pathogenesis of inflammatory bowel disease. Antioxidant enzymes, such as superoxide dismutase (SOD), are candidate drugs for modulating this pathogenic factor. This study was designed to determine the therapeutic value of SOD in an experimental model of colitis and to study the mechanisms underlying its effects on intestinal inflammation. For that purpose, colitic (trinitrobenzene sulfonic acid-induced) and control rats were studied. Groups of colitic animals were treated with different doses of SOD (1, 4, or 13 mg/kg/day) or vehicle, starting after induction of colitis and during 7 days. Clinical and pathological markers of colitis severity and lipid peroxidation in colonic tissue were measured. Leukocyte-endothelial cell interactions in colonic venules and expression of vascular cell adhesion molecule 1 (VCAM-1) were determined. Development of colitis was associated with a significant loss in body weight, an increase in macroscopic and microscopic damage scores, and colonic myeloperoxidase activity. Administration of SOD significantly attenuated these changes in a dose-dependent manner and reduced lipid peroxidation in colonic tissue. The increase in leukocyte rolling and adhesion in colonic venules of colitic rats were significantly reduced by administration of SOD, 13 mg/kg/day. Development of colitis was associated with a marked increase in endothelial VCAM-1 expression, which was significantly reduced by treatment with SOD. In conclusion, treatment with SOD significantly reduces peroxidation reactions in the inflamed colon and affords significant amelioration of colonic inflammatory changes in experimental colitis. This effect is related to a reduction in VCAM-1 expression and leukocyte recruitment into the inflamed intestine.

Animals↗