The histopathological features and the associated clinical findings of ulcerative colitis (UC) are due to persistent inflammatory response in the colon mucosa. Interventions that suppress this response benefit UC patients. We tested whether sodium arsenite (SA) benefits rats with dextran sulfate sodium (DSS)-colitis. The DSS-colitis was induced by 5% DSS in drinking water. SA (10 mg/kg; intraperitoneally) was given 8 h before DSS treatment and then every 48 h for 3 cycles of 7, 14 or 21 d. At the end of each cycle rats were sacrificed and colon sections processed for histological examination. DSS induced diarrhea, loose stools, hemoccult positive stools, gross bleeding, loss of body weight, loss of epithelium, crypt damage, depletion of goblet cells and infiltration of inflammatory cells. The severity of these changes increased in the order of Cycles 1, 2 and 3. Treatment of rats with SA significantly reduced this severity and improved the weight gain.
Animals ; Arsenites ; pharmacology ; Body Weight ; Colitis ; chemically induced ; drug therapy ; Colitis, Ulcerative ; chemically induced ; Colon ; pathology ; Dextran Sulfate ; pharmacology ; Epithelium ; pathology ; Inflammation ; Male ; Models, Biological ; Rats ; Rats, Wistar ; Sodium Compounds ; pharmacology ; Time Factors ; Treatment Outcome

It has been reported that colitis may be associated with intrarectally administered drugs or chemicals. Colonotoxicity may results from conventional medical therapy, herbal or other illicit drugs, contrast materials, and detergents. Clues that a colitis may be due to an intrarectally administered agent include perianal excoriation, segmental distal colitis due to a concentration gradient from enema administration, and recent diagnostic or therapeutic administration of high risk solutions such as hypertonic contrast agents or detergent enemas. Barium is a highly viscous contrast agent that is insoluble in water. Barium enemas are usually very safe. Also, no case report of barium-induced chemical colitis has been reported yet. We report a case of chemical colitis with colonic stricture occurring after the barium enema for diagnostic purpose.
Barium Sulfate/*adverse effects ; Colitis/*chemically induced/pathology ; Contrast Media/*adverse effects ; *Enema ; Humans ; Male ; Middle Aged

OBJECTIVES: Liver disease is the most common extra-intestinal manifestation of ulcerative colitis (UC), but the underlying pathogenesis is still not clarified. It is well accepted that the occurrence of UC-related liver disease has close correlation with immune activation, intestinal bacterial liver translocation, inflammatory cytokine storm, and the disturbance of bile acid circulation. The occurrence of UC-related liver disease makes the therapy difficult, therefor study on the pathogenesis of UC-related liver injury is of great significance for its prevention and treatment. Glutathione (GSH) shows multiple physiological activities, such as free radical scavenging, detoxification metabolism and immune defense. The synthesis and the oxidation-reduction all contribute to GSH antioxidant function. It is reported that the deficiency in hepatic GSH antioxidant function participates in multiple liver diseases, but whether it participates in the pathogenesis of UC-related liver injury is still not clear. This study aims to investigate the feature and underlying mechanism of GSH synthesis and oxidation-reduction function during the development of UC, which will provide useful information for the pathogenesis study on UC-related liver injury. METHODS: UC model was induced by 2,4,6-trinitrobenzenesulfonic acid (TNBS)-ethanol solution (5 mg/0.8 mL per rat, 50% ethanol) via intra-colonic administration in rats, and the samples of serum, liver, and colon tissue of rats were collected at the 3rd, 5th, and 7th days post TNBS. The severity degree of colitis was evaluated by measuring the disease activity index, colonic myeloperoxidase activity, and histopathological score, and the degree of liver injury was evaluated by histopathological score and the serum content of alanine aminotransferase. Spearman correlation analysis was also conducted between the degree of colonic lesions and index of hepatic histopathological score as well as serum aspartate aminotransferase level to clarify the correlation between liver injury and colitis. To evaluate the hepatic antioxidant function of GSH in UC rats, hepatic GSH content, enzyme activity of GSH peroxidase (GSH-Px), and GSH reductase (GR) were determined in rats at the 3rd, 5th, and 7th days post TNBS, and the protein expressions of glutamine cysteine ligase (GCL), GSH synthase, GSH-Px, and GR in the liver of UC rats were also examined by Western blotting. RESULTS: Compared with the control, the disease activity index, colonic myeloperoxidase activity, and histopathological score were all significantly increased at the 3rd, 5th, and 7th days post TNBS (all P<0.01), the serum aspartate aminotransferase level and hepatic histopathologic score were also obviously elevated at the 7th day post TNBS (all P<0.05). There was a significant positive correlation between the degree of liver injury and the severity of colonic lesions (P=0.000 1). Moreover, compared with the control, hepatic GSH content and the activity of GSH-Px and GR were all significantly decreased at the 3rd and 5th days post TNBS (P<0.05 or P<0.01), and the protein expressions of GCL, GSH-Px, and GR were all obviously down-regulated at the 3rd, 5th, and 7th days post TNBS (P<0.05 or P<0.01). CONCLUSIONS There is a significant positive correlation between the degree of liver injury and the severity of colonic lesions, and the occurrence of reduced hepatic GSH synthesis and decreased GSH reduction function is obviously earlier than that of the liver injury in UC rats. The reduced hepatic expression of enzymes that responsible for GSH synthesis and reduction may contribute to the deficiency of GSH synthesis and oxidation-reduction function, indicating that the deficiency in GSH antioxidant function may participate in the pathogenesis of UC related liver injury.
Animals ; Antioxidants ; Aspartate Aminotransferases ; Colitis/chemically induced* ; Colitis, Ulcerative/metabolism* ; Colon/pathology* ; Glutathione/biosynthesis* ; Liver/metabolism* ; Peroxidase/metabolism* ; Rats ; Trinitrobenzenesulfonic Acid

AIMTo investigate the effects of glutamine on the colonic mucosa of mice subjected to colitis gravis.

METHODS64 Kunming mice were divided randomly into 4 groups (n=16): healthy group: animals not subjected to colitis; model group: animals subjected to colitis gravis but without glutamine supplementation; low-Gln group: animals subjected to colitis gravis and with low dose of glutamine supplementation; high-Gln group: animals subjected to colitis gravis and with high dose of glutamine supplementation. Animals belonging to the control, the low-Gln, the high-Gin groups were subjected to coloclysis by HAC to be colitis gravis animals. When the models were established, the healthy and the control groups were given some isotonic Na chloride by intragastric administration. The low-Gln group and the high-Gln group were given the same volume but different concentration of glutamine(low-Gln group--2 mmol x Kg(-1) bw, high-Gln group--2 mmol x Kg(-1) bw) for 7 days. Then the mice were sacrificed, the pathohistological changes of the colon were observed, besides, the content of endotoxin in the blood serum, the level of counteracting oxidation and the activities of MPO of the colon tissue were determined.

RESULTSThe glutamine lessened the pathological injures in the colon and relieved the step up of the content of endotoxin in the blood serum , the step down level of counteracting oxidation and the step up activity of MPO in the colon tissue, which were caused by colitis gravis.

CONCLUSIONThe glutamine can protect the colon of mice subjected to colitis gravis.

Acetic Acid ; Animals ; Colitis, Ulcerative ; chemically induced ; drug therapy ; pathology ; Colon ; pathology ; Female ; Glutamine ; pharmacology ; therapeutic use ; Male ; Mice ; Random Allocation

Rectal enema used for diagnostic and therapeutic purposes infrequently causes colitis. In medical practice, enemas are known to incidentally bring about colitis by mechanical, thermal, or direct chemical injuries. Coffee enema is told to ameliorate the constipation in alternative medicine. We hereby report a case of acute colitis resulting from coffee enema, which was presented with severe abdominal pain and hematochezia.
Acute Disease ; Aged ; Coffee/*adverse effects ; Colitis/chemically induced/*diagnosis/pathology ; Colonoscopy ; *Enema ; Gastrointestinal Hemorrhage ; Humans ; Male ; Rectal Diseases/*diagnosis ; Tomography, X-Ray Computed

Rectal enema used for diagnostic and therapeutic purposes infrequently causes colitis. In medical practice, enemas are known to incidentally bring about colitis by mechanical, thermal, or direct chemical injuries. Coffee enema is told to ameliorate the constipation in alternative medicine. We hereby report a case of acute colitis resulting from coffee enema, which was presented with severe abdominal pain and hematochezia.
Acute Disease ; Aged ; Coffee/*adverse effects ; Colitis/chemically induced/*diagnosis/pathology ; Colonoscopy ; *Enema ; Gastrointestinal Hemorrhage ; Humans ; Male ; Rectal Diseases/*diagnosis ; Tomography, X-Ray Computed

BACKGROUND/AIMS: Saccharomyces boulardii has been reported to be beneficial in the treatment of inflammatory bowel disease. The aim of this work was to evaluate the effect of S. boulardii in a mice model of 2,4,6-trinitrobencene sulfonic acid (TNBS) induced colitis and analyze the expression of genes in S. boulardii treated mice by microarray. METHODS: BALB/c mice received TNBS or TNBS and S. boulardii treatment for 4 days. Microarray was performed on total mRNA form colon, and histologic evaluation was also performed. RESULTS: In mice treated with S. boulardii, the histological appearance and mortality rate were significantly restored compared with rats receiving only TNBS. Among 330 genes which were altered by both S. boulardii and TNBS (>2 folds), 193 genes were down-regulated by S. boulardii in microarray. Most of genes which were down-regulated by S. bouardii were functionally classified as inflammatory and immune response related genes. CONCLUSIONS: S. boulardii may reduce colonic inflammation along with regulation of inflammatory and immune responsive genes in TNBS-induced colitis.
Animals ; Colitis/chemically induced/genetics/*therapy ; Colon/metabolism/pathology ; Gene Expression Profiling ; Mice ; Mice, Inbred BALB C ; Oligonucleotide Array Sequence Analysis ; *Probiotics ; *Saccharomyces ; Trinitrobenzenesulfonic Acid

OBJECTIVETo investigate the role of mast cells and gut hormones and their interactions in TNBS-induced ulcerative colitis.

METHODSRat models of ulcerative colitis were established by a single intracolonic injection of 100 mg/kg TNBS (in 0.3 ml 50% ethanol). At 0, 6, 11, 16, 21 days after TNBS injection, the rats were sacrificed to determine the count of the mast cells. Histamine level in the whole blood, and the levels of histamine, substance P (SP), vasoactive intestinal peptide (VIP), and somatostatin (SS) in the distal colons were measured by fluorimetry or radioimmune assay. Immunofluorescence double staining was used to observe the relationship of the mast cells with SP, VIP, and SS positive nerve fibers.

RESULTSOn day 6 after TNBS injection, obvious ulcers occurred in the distal colon of the rats with significantly increased histamine level in the whole blood (P<0.05) but significantly decreased colonic histamine levels (P<0.05). The histamine levels in the whole blood and distal colon gradually recovered the normal levels. The mast cells significantly increased on day 16 (P<0.05) and maintained the high level till day 21. The distribution of mast cells was altered after TNBS injection, and the cells were found to aggregate in the myenteric region. SP levels in the distal colon significantly increased on day 11 (P<0.05) and maintained the high level till day 21. Immunofluorescence double staining revealed numerous mast cells close to the SP- and VIP-positive nerve fibers at different time points after TNBS injection. VIP positivity and the number of VIP-positive nerve fibers in the myenteric region were markedly increased, but no mast cells were observed in association with SP- and VIP-positive nerve fibers. The distribution of MC was not found to associate with the SS-positive nerve fibers.

CONCLUSIONThe mast cells and histamine released by them, as well as parasecretion of SP and VIP, participate in tissue damage by TNBS-induced colitis. Bidirectional neuroimmunomodulation of the mast cells, SP and VIP have important effect on the development of TNBS-induced colitis.

Animals ; Colitis, Ulcerative ; chemically induced ; metabolism ; pathology ; Disease Models, Animal ; Male ; Mast Cells ; secretion ; Rats ; Rats, Sprague-Dawley ; Substance P ; metabolism ; Trinitrobenzenesulfonic Acid ; toxicity ; Vasoactive Intestinal Peptide ; metabolism

Several models of experimental ulcerative colitis have been reported previously. However, none of these models showed the optimum characteristics. Although dextran sulfate sodium-induced colitis results in inflammation resembling ulcerative colitis, an obvious obstacle is that dextran sulfate sodium is very expensive. The aim of this study was to develop an inexpensive model of colitis in rats. Sprague-Dawley rats were treated with 2% dextran sulfate sodium in drinking water for 3 d followed by an intracolonic administration of 30% ethanol. The administration of 2% dextran sulfate sodium followed by 30% ethanol induced significant weight loss, diarrhea and hematochezia in rats. Severe ulceration and inflammation of the distal part of rat colon were developed rapidly. Histological examination showed increased infiltration of polymorphonuclear leukocytes, lymphocytes and existence of cryptic abscesses and dysplasia. The model induced by dextran sulfate sodium at lower concentration followed by 30% ethanol is characterized by a clinical course, localization of the lesions and histopathological features similar to human ulcerative colitis and fulfills the criteria set out at the beginning of this study.
Acute Disease ; Administration, Rectal ; Animals ; Colitis, Ulcerative ; chemically induced ; pathology ; Dextran Sulfate ; administration & dosage ; Disease Models, Animal ; Drug Administration Schedule ; Ethanol ; administration & dosage ; Female ; Rats

OBJECTIVE: To investigate the effects of deficiency of CHL1 in inflammatory bowel disease (IBD). METHODS: Dextran Sulfate Sodium (DSS)-induced colitis model was used to study the effects of deficiency of CHL1 on the development of IBD. Ten CHL1(+/+) mice in C57/BL6 background were randomly divided into CHL1(+/+) group and DSS-induced CHL1(+/+) group. Ten CHL1(-/-) mice in C57/BL6 background were randomly divided into CHL1(-/-) group and DSS-induced CHL1(-/-) group. DSS-induced CHL1(+/+) group and DSS-induced CHL1(-/-)group were fed with 1.5% DSS for 7 days, and then drinking distilled water for 2 days. CHL1(+/+) group and CHL1(-/-) group as control group were fed with distilled water for 9 days. The changes of weight, survival, fecal blood and the change of colon length in this study were observed. RESULTS: On the 7 day, the weight of DSS-induced CHL1(-/-) group were reduced significantly, and DSS-induced CHL1(-/-) group had extreme mortality on the 9th day. The fecal blood of DSS-induced CHL1(-/-) group also had higher score than that of DSS-induced CHL1(+/+) group. In the DSS-induced CHL1(-/-) group,the length of colon was shortened obviously. CONCLUSIONS The loss of CHL1 aggravates the development of IBD.
Animals ; Cell Adhesion Molecules ; deficiency ; genetics ; Colitis ; chemically induced ; genetics ; Colon ; pathology ; Dextran Sulfate ; Disease Models, Animal ; Mice ; Mice, Inbred C57BL ; Random Allocation