Transplantation of human stem cells from the apical papilla for treating dextran sulfate sodium-induced experimental colitis / 中国组织工程研究

BACKGROUND: Stem cells from the apical papilla (SCAP) play important roles in the formation and development of dental roots. However, the immune-modulating capacity of SCAP has not been fully elucidated. OBJECTIVE: To test the therapeutic effects of transplantation of SCAP on dextran sulfate sodium-induced experimental colitis. METHODS: Twenty-four C57/BL6 mice were equally divided into four groups (normal control, positive control, SCAP treatment group, and FasL-knockdown SCAP group), and latter three groups of mice were induced to acute experimental colitis by 3% dextran sulfate sodium in drinking water. At day 3 after modeling, model mice were treated with PBS, human SCAP (2×106 cells), and FasL-knockdown SCAP via intraperitoneal injection, respectively. Inflammation was evaluated by measuring body mass and length of the colon, detecting levels of interleukin 1β, interleukin 6 and tumor necrosis factor α, as well as histological analyses at day 10 after modeling. Levels of Tregs in mesenteric lymph nodes in mice were detected using flow cytometric analysis. RESULTS AND CONCLUSION: SCAP transplantation could ameliorate the inflammation in dextran sulfate sodium-induced colitis mice, and body mass loss and symptoms were significantly improved. Pathological score and the levels of three inflammatory cytokines in the colon tissue decreased significantly. Flow cytometric analysis revealed an increased level of Tregs in mesenteric lymph nodes. Knocking down of FasL gene in SCAP abrogated the therapeutic effects of SCAP in ameliorating dextran sulphate sodium-induced colitis. Therefore, Fas-FasL pathway played an important role in the underlying mechanism of the immune-modulating capacity of SCAP.

Effect of tumor necrosis factor-related apoptosis-inducing ligand gene knock-out on the gut microbiota in mice with dextran sodium sulphate induced colitis / 中华消化杂志

Objective@#To investigate the influence of tumor necrosis factor-related apoptosis-inducing ligant (TRAIL) deficiency on mice colitis and the gut microbiota composition by inclding the expermental colitis model in tumor necrosis factor-related apoptosis-inducing ligand gene knockout (TRAIL-/-) mice.@*Methods@#C57BL/6 TRAIL-/- mice and wild type (WT) mice were selected and assigned into TRAIL-/- control group (eight mice), TRAIL-/- colitis group (16 mice), WT control group (eight mice) and WT colitis group (16 mice). The mice of two colitis groups were oral administrated with 3.5% dextran sulphate sodium (DSS) in drinking water for seven consecutive days to induce experimental colitis model. The severity of colitis was evaluated by clinical appearance and histopathological examination. The colonic tissue samples of mice were collected and microbiota profile was analyzed by 16S rDNA sequencing method. USEARCH software and R language were used to analyze the difference of gut microbiota among TRAIL-/- control group, TRAIL-/- colitis group, WT control group and WT colitis group. T test and Mann-Whitney U test were used for statistical analysis.@*Results@#After modeling, the disease activity index (DAI) of WT colitis mice and TRAIL-/- colitis mice both gradually increased over time. Furthermore, compared with colitis mice, TRAIL-/- colitis mice developed body weight loss, diarrhea and hemafecia earlier. On the seventh day after modeling, the percentage of body weight loss of TRAIL-/- colitis mice and WT colitis mice was (28.98±2.84)% and (17.87±3.70)%, respectively; and the difference was statistically significant (t=9.53, P<0.01). The length of colon of TRAIL-/- colitis mice was shorter than that of WT colitis mice ((4.63±0.28) cm vs. (6.02±0.41) cm), and the difference was statistically significant (t=11.20, P<0.01). The DAI of TRAIL-/- colitis mice was higher than that of WT colitis mice (3.00±0.00 vs. 2.32±0.05), and the difference was statistically significant (t=54.40, P<0.01). The histological score of TRAIL-/- colitis mice was higher than that of WT colitis mice (6.19±0.25 vs. 3.87±0.22), and the difference was statistically significant (t=27.87, P<0.01). Under the microscope, colonic mucosal epithelial injury, crypt structure destruction and inflammatory cell infiltration were more obvious in TRAIL-/- colitis mice than in WT colitis mice. The alpha diversity of colonic flora was more significant in TRAIL-/- colitis group compared with that of WT colitis group. At the family level, the relative richness of Deferribacteraceae, Ruminococcaceae, Rikenellaceae, F16 and Paraprevotellaceae significantly increased in TRAIL-/- colitis group, but the relative richness of Enterococcaceae obviously reduced ((19.839±19.991)% vs. (7.224±11.241)%, (3.564±2.543)% vs.(2.861±3.821)%, (0.123±0.066)% vs. (0.068±0.049)%, (0.032±0.033)% vs. (0.006±0.011)%, (0.153±0.098)% vs. (0.062±0.054)% and (0.013±0.027)% vs. (0.054±0.121)%, respectively; U=51, 69, 53, 35, 49 and 69, respectively; P<0.01 and 0.05, respectively). In addition, at the genus level the relative richness of Oscillospira, Mucispirillum and Cytophaga in TRAIL-/- colitis group remarkably elevated, and the relative richness of Enterococcus significantly decreased ((2.363±2.147)% vs. (1.813±2.847)%, (19.839±19.991)% vs. (7.223±11.241)%, (0.104±0.153)% vs. (0.046±0.069)% and (0.076±0.049)% vs. (0.135±0.074)%, respectively; U=70, 51, 66 and 65, respectively; P <0.05 and 0.01, respectively).@*Conclusion@#TRAIL deficiency aggravate DSS-induced colitis, and increase the alpha diversity of colonic microbiota in colitis mice.

Effect of tumor necrosis factor-related apoptosis-inducing ligand gene knock-out on the gut microbiota in mice with dextran sodium sulphate induced colitis / 中华消化杂志

Objective To investigate the influence of tumor necrosis factor-related apoptosis-inducing ligant (TRAIL) deficiency on mice colitis and the gut microbiota composition by inclding the expermental colitis model in tumor necrosis factor-related apoptosis-inducing ligand gene knockout ( TRAIL-/-) mice. Methods C57BL/6 TRAIL-/-mice and wild type (WT) mice were selected and assigned into TRAIL-/-control group (eight mice), TRAIL-/-colitis group (16 mice), WT control group (eight mice) and WT colitis group (16 mice).The mice of two colitis groups were oral administrated with 3.5% dextran sulphate sodium (DSS) in drinking water for seven consecutive days to induce experimental colitis model .The severity of colitis was evaluated by clinical appearance and histopathological examination .The colonic tissue samples of mice were collected and microbiota profile was analyzed by 16S rDNA sequencing method.USEARCH software and R language were used to analyze the difference of gut microbiota among TRAIL-/-control group, TRAIL-/-colitis group, WT control group and WT colitis group .T test and Mann-Whitney U test were used for statistical analysis . Results After modeling, the disease activity index (DAI) of WT colitis mice and TRAIL-/-colitis mice both gradually increased over time .Furthermore, compared with colitis mice, TRAIL-/-colitis mice developed body weight loss, diarrhea and hemafecia earlier .On the seventh day after modeling , the percentage of body weight loss of TRAIL-/-colitis mice and WT colitis mice was (28.98 ±2.84)%and (17.87 ±3.70)%, respectively; and the difference was statistically significant (t＝9.53, P?0.01).The length of colon of TRAIL-/-colitis mice was shorter than that of WT colitis mice ((4.63 ±0.28) cm vs.(6.02 ±0.41) cm), and the difference was statistically significant (t＝11.20, P?0.01).The DAI of TRAIL-/-colitis mice was higher than that of WT colitis mice (3.00 ±0.00 vs.2.32 ±0.05), and the difference was statistically significant (t ＝54.40, P? 0.01).The histological score of TRAIL-/-colitis mice was higher than that of WT colitis mice (6.19 ±0.25 vs. 3.87 ±0.22), and the difference was statistically significant (t ＝27.87, P?0.01).Under the microscope, colonic mucosal epithelial injury , crypt structure destruction and inflammatory cell infiltration were more obvious in TRAIL-/-colitis mice than in WT colitis mice.The alpha diversity of colonic flora was more significant in TRAIL-/-colitis group compared with that of WT colitis group .At the family level, the relative richness of Deferribacteraceae, Ruminococcaceae, Rikenellaceae, F16 and Paraprevotellaceae significantly increased in TRAIL-/-colitis group, but the relative richness of Enterococcaceae obviously reduced ((19.839 ±19.991)%vs. (7.224 ±11.241)%, (3.564 ±2.543)% vs.(2.861 ±3.821)%, (0.123 ±0.066)% vs.(0.068 ± 0.049)%, (0.032 ±0.033)% vs.(0.006 ±0.011)%, (0.153 ±0.098)% vs.(0.062 ±0.054)% and (0.013 ±0.027)%vs.(0.054 ±0.121)%, respectively; U＝51, 69, 53, 35, 49 and 69, respectively; P? 0.01 and 0.05, respectively).In addition, at the genus level the relative richness of Oscillospira, Mucispirillum and Cytophaga in TRAIL-/-colitis group remarkably elevated , and the relative richness of Enterococcus significantly decreased ((2.363 ±2.147)% vs.(1.813 ±2.847)%, (19.839 ±19.991)% vs.(7.223 ± 11.241)%, (0.104 ±0.153)%vs.(0.046 ±0.069)% and (0.076 ±0.049)% vs.(0.135 ±0.074)%, respectively; U＝70, 51, 66 and 65, respectively; P ?0.05 and 0.01, respectively).Conclusion TRAIL deficiency aggravate DSS-induced colitis, and increase the alpha diversity of colonic microbiota in colitis mice .

Therapeutic Effects of Sinomenine on Trinitrobenzene Sulfonic Acid-induced Chronic Colitis in Mice / 中国药师

Objective:To evaluate the therapeutic effects of sinomenine on T-helper cell type 1-mediated experimental colitis in-duced by 2,4,6-trinitrobenzene sulfonic acid (TNBS) in mice. Methods:Balb/c mice were divided into five groups:ethanol control group, TNBS model group, and sinomenine treatment groups (50, 100 and 200 mg·kg-1 ) with 10 ones in each. Colitis was induced by colonic instillation of TNBS dissolved in 0. 1 ml of 50% ethanol. Seven days after the colonic instillation of TNBS, sinomenine was given by gastric gavage once daily for 21 days. The mice were sacrificed on the 28th day, the injury degree of colonic mucosa was ob-served, the colon myeloperoxidase ( MPO) activity was determined, and the levels of inflammatory cytokines ( TNF-α, IL-17 and IL-23) were determined by ELISA. Results:Compared with those in TNBS model group, the body mass, gross injury score and histologi-cal findings in sinomenine groups at medium dose and high dose were significantly improved (P<0. 05), the activity of MPO signifi-cantly decreased (P<0. 05), and the protein levels of TNF-α, IL-17 and IL-23 in colonic mucosa were lower than those in TNBS group (P<0. 05). Conclusion:Sinomenine has notable therapeutic effect on TNBS-induced chronic colitis in mice, and the mecha-nism is related to the inhibition of Th1 cytokines by sinomenine.

Investigation of pulmonary involvement in inflammatory bowel disease in an experimental model of colitis

BACKGROUND/AIMS: Inflammatory bowel disease (IBD) may also involve various extra-intestinal organs. Clinical studies have found asymptomatic/symptomatic pulmonary involvement in 1% to 6% of patients with IBD. The present study histopathologically investigated pulmonary involvement in an experimental model of colitis in order to demonstrate pulmonary tissue involvement in IBD and to expose potential etiological factors. It also explored the relation between inflammation and tissue concentrations of vascular endothelial growth factor (VEGF) and tumor necrosis factor α (TNF-α). METHODS: The study comprised 24 male Wistar albino rats. The rats were divided into four groups of six rats each. Acute colitis was induced in two separate groups using either the dextran sulphate sodium (DSS) or trinitrobenzene sulfonic acid (TNBS) method, while the other two groups were used as controls for each model of colitis. Wallace scoring was used for macroscopic assessment of colitis, and the lungs were histopathologically examined. Concentrations of VEGF and TNF-α in pulmonary tissue were measured by the enzyme-linked immunosorbent assay method. RESULTS: The number of animals that had alveolar hemorrhage was significantly higher in the TNBS-induced colitis and DSS-induced colitis groups compared to their own control groups (p = 0.015 and p = 0.015, respectively). VEGF and TNF-α concentrations in pulmonary tissues were significantly increased in both the TNBS colitis and DSS colitis groups compared to their own control groups (p = 0.002 and p = 0.004, respectively; and p = 0.002 and p = 0.002, respectively). CONCLUSIONS: The present study demonstrated that significant and serious histopathological changes directly associated with colitis occur in the lungs in IBD.

Effect of Pentoxifylline on Experimental-dextran Sulphate Sodium-induced Colitis in Rats.

Aims: Ulcerative colitis (UC) is considered as an idiopathic, chronic inflammatory bowel disease (IBD) with multifactorial agents. Tumor necrosis factor-alpha (TNF-α) has been suggested to be one of them. The study was designed to evaluate whether pentoxifylline (PTX), as TNF-α suppressor, has a beneficial effect in rats with dextran sulfate sodium (DSS) induced-colitis. Study Design: Original research papers. Place and Duration of Study: In both Anatomy Department, Faculty of Medicine, Menoufia University and Animal medicine & Infectious Diseases Department, Faculty of Veterinary Medicine Sadat City Branch , Menoufia University, Egypt , between April 2009 and August 2010. Methodology: Fifty adult male rats were divided randomly and equally into: control group, model control group, colitis model group, PTX treated group and recovery group. Induction of colitis was made in colitis model by adding DSS to the drinking water; for three weeks (5% for one week followed by 3% of for two weeks). Rats in both PTX treated and model control groups received pentoxifylline for two weeks after the induction of colitis; by intraperitoneal injection (100 mg/kg/day; 1ml /rat). Colon mucosal inflammation and damage were assessed through; clinical, macroscopic, microscopic, morphometric and molecular assessments. Results: Rats treated with oral administration of DSS for three weeks developed clinical and macroscopic signs of colitis. Treatment with PTX for two weeks, in the treated group or cessation of DSS for two weeks, in the recovery group relieved the colitis symptoms including: diarrhea, reduction in body weight, shortening and ulceration of the colon and extensive colonic damage. All of these were associated with a significant increase in TNF-α m RNA expression. However, an improvement was more significant among treated animals than that in the recovery one. Conclusion: Pentoxyfylline seems to be an effective in the treatment of ulcerative colitis for further investigation. Also, the unclear dual role of mast cell in both induction and treatment of the disease should be considered in a further investigation.

Evaluation of sucralfate enema in experimental diversion colitis / Avaliação dos efeitos da aplicação de enemas com sucralfato em modelo experimental de colite de exclusão

Diversion colitis (DC) is an inflammatory disease that develops in segments with fecal diversion. Sucralfate (SCF) complex, which consists of sucrose octasulfate and polyaluminum hydroxide, has been demonstrated to be effective in the treatment of different forms of colitis. However, until now, the effects of SCF have not been evaluated in DC. OBJECTIVE: to evaluate whether the use of enemas containing SFC improves histological findings in experimental DC. METHODS: Thirty-six rats underwent right colon bypass procedure through the creation of a proximal colostomy and a distal mucous fistula. The animals were divided into two groups according to the euthanization procedure to be performed two to four weeks after surgery. Each experimental group was divided into three subgroups of six animals, which were submitted to daily application of enemas containing saline solution 0.9% or SCF at concentrations of 1.0 g/kg/day or 2.0 g/kg/day, respectively. The diagnosis of DC in segments with fecal diversion was established by histopathological study considering the following variables: epithelial loss, formation of crypt abscesses, the population of goblet cells, inflammatory infiltrate and presence of fibrosis. For statistical analysis, the nonparametric Mann-Whitney and Kruskal-Wallis tests were used, with a significance level of 5% (p <0.05). RESULTS: It was observed that the daily application of SCF enemas decreased epithelial loss, formation of colon crypt abscesses, inflammatory infiltrate and tissue fibrosis (p <0.05), unrelated to time of intervention. The intervention with SCF preserves the goblet cell population. The effects of the substance on the preservation of colonic epithelium; the decrease in the inflammatory process and subsequent abscess formation in the colon crypts are associated with the concentration used, whereas tissue fibrosis decrease is associated with the concentration and time of intervention. CONCLUSION: Preventive application of SCF enemas reduces the inflammatory process in the colon with fecal diversion. (AU)

A colite de exclusão (CE) é uma doença inflamatória que se desenvolve em segmentos desprovidos de trânsito fecal. O sucralfato (SCF) complexo formado pelo octossulfato de sacarose e hidróxido de polialumínio vem se demonstrando eficaz para o tratamento de diferentes formas de colite, porém, até a presente data, os efeitos do SCF ainda não foram avaliados na CE. OBJETIVO: avaliar se a aplicação de clisteres contendo SFC melhora as alterações histológicas encontradas em modelo experimental de CE. MÉTODOS: trinta e seis ratos foram submetidos à derivação do trânsito no cólon direito pela confecção de colostomia proximal e fístula mucosa distal. Os animais foram divididos em dois grupos experimentais de acordo com o sacrifício ser realizado após duas ou quatro semanas do procedimento cirúrgico. Cada grupo experimental foi dividido em três subgrupos de seis animais segundo terem sidos submetidos à aplicação diária com enemas contendo solução fisiológica a 0,9% ou SCF nas concentrações de 1,0g/kg/dia ou 2,0 g/kg/dia. O diagnóstico de CE nos segmentos sem trânsito foi estabelecido por estudo histopatológico considerando-se as seguintes variáveis: perda epitelial, formação de abscessos nas criptas, população de células caliciformes, infiltrado inflamatório e a presença de fibrose. Para análise estatística adotou-se os testes não paramétricos de Mann-Withney e Kruskal-Wallis estabelecendo-se para ambos, nível de significância de 5% (p < 0,05). RESULTADOS: verificou-se que a aplicação diária de enemas com SCF diminui a perda epitelial, a formação de abscessos nas criptas cólicas, o infiltrado inflamatório e a presença de fibrose tecidual (p < 0,05), não relacionada ao tempo de intervenção. A intervenção com SCF preserva a população de células caliciformes. Os efeitos da substância na preservação do epitélio cólico, na redução do processo inflamatório e consequente formação de abscessos nas criptas cólicas encontram-se relacionado à concentração utilizada, enquanto a redução da fibrose tecidual a concentração e ao tempo de intervenção. CONCLUSÃO: a aplicação preventiva de enemas com SCF reduz o processo inflamatório em segmentos cólicos desprovidos de transito intestinal. (AU)

Efficacy of Setarud (IMOD®), a novel drug with potent anti-toxic stress potential in rat inflammatory bowel disease and comparison with dexamethasone and infliximab.

The inflammatory bowel disease (IBD) is an idiopathic, immune-mediated and chronic intestinal condition. In the present study, the effect of Serarud (IMOD®), a novel natural drug with known immunomodulatory, anti-inflammatory and antioxidant properties was investigated in experimental colitis in rats and compared with the dexamethasone and infliximab. Immunologic colitis was induced by intracolonic administration of a mixture of trinitrobenzene sulfonic acid (TNBS) and absolute ethanol in male Wistar rats. Animals were divided into 6 groups of sham (normal group), control (vehicle-treated), positive control (dexamethasone 1 mg/kg/day given orally and infliximab 5 mg/kg/day given subcutaneously) and 3 Setarud-treated groups (13.3, 20, 30 mg/kg/day given intraperitoneally). The treatment continued for 14 consecutive days and then animals were decapitated on the day 15 and distal colons were removed for macroscopic, microscopic, and biochemical assays. Biochemical markers, including TNF-, IL-1, ferric reducing/antioxidant power (FRAP), myeloperoxidase (MPO) activity and thiobarbitoric acid-reactive substance (TBARS) were measured in the homogenate of colonic tissue. A remarkable reduction in macroscopic and histological damage scores was observed in the animals treated with Setarud. These findings were confirmed by decreased levels of TNF-, interleukin-1, MPO activity and TBARS, and raised levels of FRAP in the colon tissue. These observations confirmed the immunomodulatory, anti-inflammatory and antioxidant properties of Setarud in experimental colitis, which was comparable to those of dexamethasone and infliximab.

Role of mucins secretion in the process that bifid triple viable capsule attenuates the recurrence of murine experimental colitis / 中华临床营养杂志

Objective To investigate the role of mucins secretion in the process that bifid triple viable capsule attenuates the recurrence of murine experimental colitis. Methods Mice were randomly allocated into BIFICO group (gavage with bifid triple viable capsule), 2,4,6-trinitrobenzenesulfonic acid (TNBS) group (gavage with phosphate-buffered saline), and normal control group. Intrarectal TNBS/ethanol challenge was given to mice on Day 0 followed by rechallenge on Day 5 ( 125 mg/kg and 180 mg/kg, respectively). On Day 5 several mice in both groups were randomly sacrificed before the second TNBS challenge and the remaining mice were sacrificed on Day 7. Disease activity index (DAI) was measured throughout the experiment. Inflammatory score was evaluated and MUC2 expression was determined using immunohistochemistry method. Results Recurrence of colitis was successfully simulated by challenging mice with two times of TNBS/ethanol solution. Compared with the TNBS group, DAI ( 1.39 ± 0. 68 vs. 2.39 ± 0.73, P = 0.003) and inflammatory score (2. 11 ± 0.78 vs. 3.22 ± 0. 97,P =0.03) were significantly decreased in BIFICO group after the second TNBS challenge. BIFICO administration significantly increased MUC2 expression (8. 67 ± 0. 87 vs. 7.86 ± 1.10, P = 0. 042 ) in BIFICO group compared with TNBS group before the second TNBS challenge. Conclusion Bifid triple viable capsule may enhance mucosal barriers by promoting mucins secretion, and thus attenuates the recurrence of murine colitis.

Probiotics in the treatment of experimental colitis in rats and its influence on T cell subsets / 中国实用内科杂志

Objective To evaluate the effects of probiotics in experimental colitis of rats.Methods Models of experimental colitis were established.Several groups of rats were set up as probiotics group,negative group and positive group.Histologic scoring was used to estimate effects of drugs;the expression of CD~+_4 andCD~+_8 on T cell surface in peripheral blood,spleen mononuclear cells and intraepithelial lymphocytes of colon were detected by flow cytometry.Results Histopathology shows that probiotics of larger dosage was curative for experimental colitis in rats.Proportion of CD~+_4 and CD~+_8 T cells increased in colon of colitis,which was decreased by treatment of larger dose of probiotics.CD~+_4/CD~+_8 ratio and T cell subsets in systemic immune system were not influenced by probiotics.Conclusion Probiotics of large dosage are effective in the treatment of experimental colitis of rats incuced by TNBS,possibly associated with immune regulation and tends to be localized in mucosal immune system in colon.

Effects of Intestinal Trefoil Factor on Colonic Mucosa in Experimental Colitis of Rats / 华中科技大学学报（医学）（英德文版）

Summary: In order to investigate the protective effects of intestinal trefoil factor (ITF) on colonic mucosa in experimental colitis of rats, ITF was detected by RT-PCR and immunohistochemistry at different time points. Three days after colitis induction, rats were treated with either 0.9 % saline solution or rhITF. Pathological changes and the expression of iNOS mRNA, NO, MDA and SOD were measured respectively. It was found that ITF was mainly located in goblet cells, significantly higher in model group than in normal group (P<0.05). rhITF could increase the iNOS mRNA expression and NO contents, and there was statistically significant difference between rhITF group and model group (P<0.05). rhITF also caused an increase of MDA and a decrease of SOD, but there was no significant difference between two groups. These results indicated that ITF has apparent therapeutic effects in ulcerative colitis, which may be associated with iNOS and NO.

Effect of Atorvastatin, a HMG-CoA Reductase Inhibitor, in Experimental Colitis in Mice

BACKGROUND: The statins, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, are approved for cholesterol reduction, and may also be beneficial in the treatment of inflammatory disease. In this study, atorvastatin was tested in experimental colitis, a disease model of inflammatory bowel disease. METHODS: To induce colitis, dextran sodium sulfate (DSS) or trinitrobenzene sulfonic acid (TNBS) were administrated to C57BL/6 or BALB/c mice. Mice were monitored daily for loss of body weight and survival for indicated days. Colon length and histology were examined after sacrifice. RESULTS: The administration of DSS induced marked colonic inflammation and shortening, and resulted in a loss of body weight. DSSinduced colitis was not affected by atorvastatin treatment, but in contrast, the administration of atorvastatin relieved TNBS-induced colitis with a resultant rapid recovery of weight loss and a reduction in colonic length shortening. Histologically, inflammatory cell infiltration in the colonic wall, mucosal ulceration and crypt disruption were also suppressed in atorvastatin treated mice. CONCLUSION: These results suggest that atorvastatin preserves intestinal integrity in colitis, probably via the modulation of Th cell-mediated immune response, in a manner independent of innate immunity.

Effects and mechanism of celecoxib on rat colitis induced by trinitrobenzene sulfonic acid / 中华消化杂志

Objective An investigation was conducted to assess the effects and mechanism of celecoxib [a selective cyclooxygenase(COX) 2 inhibitor] on a rat colitis model induced by trinitrobenzene sulfonic acid (TNBS). Methods The rats were divided into four groups. Group 1 and group 2 were experimental groups. Group 3 and group 4 were control groups. Colitis was induced by intracolonic administration of TNBS (25 mg/ml) in a vehicle of 50% ethanol (0.25 ml) in rats of experiment groups. Three hours before induction of colitis ,the rats were beginning and continuing to treat orally with celecoxib (1.25 mg/kg, group 1) and distilled water (1 ml/0.3 kg, group 2) twice per day for 7 days , respectively. The rats in group 4 were treated orally with celecoxib (1.25 mg/kg) twice per day for 7 days. Group 3 served as healthy control. All rats that survived until the end of the experiment (7 d) were killed and the severity of damage were assessed. The prostaglandin E2 (PGE2) concentrations of colonic mucosa were tested by radioimmunoassay. Results The colonic damage scores were 11.15?3.3 in group 1 and 8.50?2.82 in group 2. Both were significantly higher than that of group 3 (0.62?0.09)( P

The role of zinc sulfate solution enema on trinitrobenzenesulphonic acid-induced colitis in rats / 中华消化杂志

Objective Zinc sulfate has anti inflammatory action in many animal models, however, the effects of zinc in colitis remained uncertain. The present study was to evaluate the role of zinc sulfate in experimental colitis and probe into its underlying mechanisms. Methods Colitis was induced by administrating 2,4,6 trinitrobenzenesulphonic acid (TNB) rectally in Spragur Dawley female rats. Beginning at the first day of TNB colitis, the rats were treated with zinc sulfate enema once daily for 6 days. The rats were sacrificed at days 8. The effects of zinc sulfate were evaluated by examining mucosal lesion area, mucosal myeloperoxidase (MPO) and superoxide dismutase (SOD) activities, mucosal prostaglandin E 2(PGE 2) and leukotriene B 4(LTB 4) levels. Results TNB induced severe colitis as evidenced by increased mucosal lesion area, mucosal MPO activity and PGE 2 and LTB 4 levels. Six days after the application of the zinc sulfate enema, the mucosal lesion area, MPO activity, PGE 2 and LTB 4 levels were all decreased significantly, except mucosal SOD activity that was remained unchanged after zinc treatments. Conclusions The data suggest that zinc sulfate enemas have an anti inflammatory action on experimental colitis through the mechanism other than increasing SOD activity.

The role of CD8~+CD28~- T suppressor cells in rats with the experimental colitis induced by 2,4-dinitrofluorobenzene / 中华消化杂志

0.05 ). But CD8 +CD28 -T suppressor cells from colitis rats was significantly higher than that from controls (spleen: 11.3% ? 2.3% vs. 5.6% ? 1.0% ; colon: 6.5% ?5.4% vs. 1.1 %? 0.6% , P 0.05 ; colon: 7.5% ? 4.2% vs. 16.9% ? 4.1% , P

The Change of CD_4~+CD_(25)~+ and CD_8~+CD_(28)~- T Regulatory Cells in Rats with the Experimental Colitis Induced by TNBS / 中国医师杂志

Objective To explore the change and function of CD 4 +CD 25 + and CD 8 +CD 28 -T regulatory cells in peripherel blood monocyte cell (PBMC), spleen and colon in rat experimental colitis induced by trinitrobenzenesulfonic acid (TNBS) . Methods The rat model of experimental colitis was established by enema with TNBS/ethanol. The proportion of CD 4 +CD 25 + and CD 8 +CD 28 - T regulatory cells in PBMC, spleen and colon was determined by flow cytometry at the first and third weeks after establishing model, respectively. Results The model of experimental colitis in rats was successfully established(n=15). Compared with control group, the proportion of CD 8 +CD 28 -T regulatory cells significantly increased in colon at the first week after establishing model [(12.7?5.4)% versus(3.87?3.7)%,P

The research on bifidobacterium inhibits inflammatory response in murine experimental colitis / 中华消化杂志

Objective To investigate the effect of bifidobacterium (Bif) supplementation on acute inflammatory response in murine dextran sulfate sodium(DSS)-induced colitis, and its possible mechanism. Methods Mice were divided into four groups: control,DSS, salfasalazine (SASP) and Bif. The mice in groups DSS, SASP and Bif were fed with 5% DSS(w/v) solution for 7 days to induce colitis, and disease activity index (DAI) was calculated every day. The mice in group SASP were fed with SASP every day during inducing colitis, and the mice in Bif group were given Bif by oral gavage from 7 days before the experiment to the end of experiment. The expression of TNF-?、NF-?B P65 and myeloperoxidase (MPO) in inflamed colon of each group was measured at the end of experiment. Results The mice in groups SASP and Bif showed a lower DAI than those in group DSS since the forth day to the end of experiment. There were lower level of TNF-? and MPO in murine inflammatory colon, and lower NF-?B P65 expression in nuclei of inflammatory cells in groups SASP and Bif than those in control at the end of experiment. Conclusions Treatment with Bif can effectively inhibit proinflammatory cytokine secretion and NF-?B activation in inflammatory cells, and decrease colonic inflammatory response in DSS induced colitis.