Protective Effect of Lactulose on Dextran Sulfate Sodium-Induced Colonic Inflammation in Rats

Rumi, G; Tsubouchi, Ryouichi; Okayama, Mitsuaki; Kato, Shinichi; Mózsik, Gyula; Takeuchi, Koji

doi:10.1023/b:ddas.0000042248.48819.ad

Cited by 78 publications

(34 citation statements)

References 34 publications

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“…This finding supports other studies that have demonstrated that certain fermentable carbohydrates may protect against intestinal inflammation and reduce the symptoms of IBD patients [7,8,38]. Prebiotics are emerging as having important nutritional benefits in both healthy and disease states and further research into the mechanisms behind their actions are required to enable understanding of the full effects.…”

Section: Discussionsupporting

confidence: 87%

Fructo-oligosaccharide Reduces Inflammation in a Dextran Sodium Sulphate Mouse Model of Colitis

2006

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Fructo-oligosaccharide (FOS) is a prebiotic that stimulates the colonic growth of bifidobacteria to promote intestinal health. This study assessed whether FOS can reduce intestinal damage associated with ulcerative colitis and accelerate recovery in a mouse model. C57BL/6 mice received 2% dextran sulphate sodium for 7 days (days 8-14). FOS (1.5 g/mL) treatment was administered twice daily (n=10/group): before and during colitis (days 1-14); during colitis (days 10-14); and during colitis and the recovery period (days 10-19). Disease activity was scored daily and colonic damage was assessed by histological analysis. FOS treatment significantly reduced disease activity and damage in the distal colon (P < .05). Treatment with FOS (days 10-14) had increased crypt depth (116+/-6 microm) compared to water treatment (90+/-4 microm, P < .05). FOS treatment (days 10-19) produced a faster recovery from damage with increased crypt depth and crypt area. These results demonstrate the protective effect of FOS treatment.

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Section: Discussionsupporting

confidence: 87%

Fructo-oligosaccharide Reduces Inflammation in a Dextran Sodium Sulphate Mouse Model of Colitis

2006

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“…The DAI was determined macroscopically by an observer unaware of the treatment the mice had received according to previously reported criteria (34). Briefly, the DAI was calculated as the sum of the diarrheal stool score (0, normal stool; 1, mildly soft stool; 2, very soft stool; and 3, watery stool) and the bloody stool score (0, normal color stool; 1, brown color stool; 2, reddish color stool; and 3, bloody stool).…”

Section: Development Of Dss-induced Colitis and Measurement Of Colon mentioning

confidence: 99%

“…The amounts of TBARS in the colonic tissues were measured as described previously (35,38). After 7 days of DSS treatment, animals were placed under deep ether anesthesia and killed.…”

Section: Lipid Peroxidation Measured By Thiobarbituric Acid-reactive mentioning

confidence: 99%

Genetic Evidence for a Protective Role for Heat Shock Factor 1 and Heat Shock Protein 70 against Colitis

Tanaka

Namba

Arai

et al. 2007

Journal of Biological Chemistry

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131

126

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Inflammatory bowel disease (IBD) involves infiltration of leukocytes into intestinal tissue, resulting in intestinal damage induced by reactive oxygen species (ROS). Pro-inflammatory cytokines and cell adhesion molecules (CAMs) play important roles in this infiltration of leukocytes. The roles of heat shock factor 1 (HSF1) and heat shock proteins (HSPs) in the development of IBD are unclear. In this study, we examined the roles of HSF1 and HSPs in an animal model of IBD, dextran sulfate sodium (DSS)-induced colitis. The colitis worsened or was ameliorated in HSF1-null mice or transgenic mice expressing HSP70 (or HSF1), respectively. Administration of DSS up-regulated the expression of HSP70 in colonic tissues in an HSF1-dependent manner. Expression of pro-inflammatory cytokines and CAMs and the level of cell death observed in colonic tissues were increased or decreased in DSS-treated HSF1-null mice or transgenic mice expressing HSP70, respectively, relative to control wild-type mice. Relative to macrophages from control wildtype mice, macrophages prepared from HSF1-null mice or transgenic mice expressing HSP70 displayed enhanced or reduced activity, respectively, for the generation of pro-inflammatory cytokines in response to lipopolysaccharide stimulation. Suppression of HSF1 or HSP70 expression in vitro stimulated lipopolysaccharide-induced up-regulation of CAMs or ROS-induced cell death, respectively. This study provides the first genetic evidence that HSF1 and HSP70 play a role in protecting against DSS-induced colitis. Furthermore, this protective role seems to involve various mechanisms, such as suppression of expression of pro-inflammatory cytokines and CAMs and ROS-induced cell death. Inflammatory bowel disease (IBD),2 Crohn disease, and ulcerative colitis have become substantial health problems with an actual prevalence of 200 -500 cases/100,000 people in western countries, which almost double every 10 years (1). Although the etiology of IBD is not yet fully understood, recent studies suggest that IBD involves chronic inflammatory disorders in the intestine because of "a vicious cycle." Infiltration into intestinal tissues causes intestinal mucosal damage induced by reactive oxygen species (ROS) that are released from the activated leukocytes, and this intestinal mucosal damage further stimulates the infiltration of leukocytes (2). To understand the molecular mechanism underlying the pathogenesis of IBD and to develop new types of clinical drugs for IBD, identification of endogenous factors that positively or negatively affect the development of IBD is important. For this purpose, various experimental animal colitis models, in particular the dextran sulfate sodium (DSS)-and trinitrobenzenesulfonic acid-induced colitis models, have been used (3).Pro-inflammatory cytokines play an important role in the activation and infiltration of leukocytes that are associated with IBD. This conclusion is supported by a range of evidence. Increases in the levels of various pro-inflammatory cytokines (such as tumor necr...

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“…19 Prebiotics are defined as Bnondigestible dietary supplements that have the ability to alter the intestinal flora and stimulate growth of native and probiotic bacteria.^2 0 Prebiotics, such as germinated barley foodstuff and lactulose, have been reported to decrease the severity of DSS-colitis. 21,22 In a clinical setting, inulin has been demonstrated to reduce the extent of inflammation in patients with pouchitis. 23 The prebiotic, fructooligosaccharide (FOS), is a nondigestible oligosaccharide with the capacity to increase intestinal concentrations of Lactobacilli and Bifidobacterium species.…”

mentioning

confidence: 99%

Prebiotic and Synbiotic Fructooligosaccharide Administration Fails to Reduce the Severity of Experimental Colitis in Rats

Geier¹,

Butler²,

Giffard³

et al. 2007

Diseases of the Colon &Amp; Rectum

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Opposing effects of the prebiotic, fructooligosaccharide, have been reported in experimental colitis. We compared the effects of the prebiotic, fructooligosaccharide, alone and in synbiotic combination with Lactobacillus fermentum BR11, on the development of dextran sulfate sodium-induced colitis in rats. Rats consumed an 18 percent casein-based diet or diet supplemented with 6 percent fructooligosaccharide or maltodextrin for 14 days. The synbiotic group was gavaged 1 ml of L. fermentum BR11 (1x10(9) cfu/ml) twice daily. From Days 7 to 14, colitis was induced via 3 percent dextran sulfate sodium in drinking water. Disease activity was assessed daily, and at killing, gastrointestinal organs were measured, weighed, and examined by quantitative histology, proliferating cell nuclear antigen immunohistochemistry, and colonic myeloperoxidase activity. Administration of dextran sulfate sodium resulted in an increased colitic disease activity, and an increased colon and cecum weight compared with normal controls. Colon and cecum weights were further increased in dextran sulfate sodium+fructooligosaccharide (colon: 19 percent; cecum: 48 percent) and dextran sulfate sodium+fructooligosaccharide/L. fermentum BR11-treated rats (16 and 62 percent) compared with dextran sulfate sodium+vehicle-treatment. Dextran sulfate sodium+fructooligosaccharide-treated rats displayed an 81 percent increase in colonic myeloperoxidase activity compared with dextran sulfate sodium-treated controls. Histologic damage severity scores increased in dextran sulfate sodium+vehicle, dextran sulfate sodium+fructooligosaccharide, and dextran sulfate sodium+fructooligosaccharide/L. fermentum BR11-treated rats compared with normal controls (P<0.05). Crypt depth increased in all treatments compared with normal controls (P<0.01). No protection from dextran sulfate sodium-colitis was accorded by fructooligosaccharide alone or in synbiotic combination with L. fermentum BR11, whereas fructooligosaccharide actually increased some indicators of colonic injury.

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Protective Effect of Lactulose on Dextran Sulfate Sodium-Induced Colonic Inflammation in Rats

Cited by 78 publications

References 34 publications

Fructo-oligosaccharide Reduces Inflammation in a Dextran Sodium Sulphate Mouse Model of Colitis

Fructo-oligosaccharide Reduces Inflammation in a Dextran Sodium Sulphate Mouse Model of Colitis

Genetic Evidence for a Protective Role for Heat Shock Factor 1 and Heat Shock Protein 70 against Colitis

Prebiotic and Synbiotic Fructooligosaccharide Administration Fails to Reduce the Severity of Experimental Colitis in Rats

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