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PubMed1983

Chemical modification of potassium channel gating in frog myelinated nerve by trinitrobenzene sulphonic acid.

We investigated the actions of externally applied trinitrobenzene sulphonic acid (TNBS) on the K currents of voltage-clamped frog myelinated nerve fibres. TNBS treatment irreversibly slowed the tail currents for K channel closing up to 10-fold. Time constants for the tail currents appear shifted 60-80 mV in the hyperpolarizing direction following TNBS treatment. The time course of K channel opening was unaffected for depolarizing pulses to potentials positive to -20 mV. For smaller pulses to potentials between -80 and -30 mV the activation time course was slower following TNBS treatment. TNBS had little or no effect on the steady-state conductance-voltage relation of K channels determined from tail current amplitude. The instantaneous current-voltage relation for K channels and potency of block by external TEA were unaffected by TNBS. K tail currents showed fast and slow components both before and after TNBS treatment. Reaction with TNBS caused the fast component to decline in amplitude and the slow component to increase both in magnitude and time constant. The rate of reaction increased with increasing pH. Full expression of altered K channel kinetics depends upon the ionic composition of the external solution. Tail currents were up to 10-fold slower when measured in 117.5 mM-K than when measured with 80% of the external K replaced by Na. The differential effects of TNBS on K channel closing and opening were modelled in a three-state kinetic scheme, with an increase in the energy barrier for closing an open channel following TNBS treatment.

Animals↗
PubMed1988

Calcium-independent increase of transmitter release at frog end-plate by trinitrobenzene sulphonic acid.

1. Application of an amino-residue-modifying reagent, 2,4,6-trinitrobenzene-1-sulphonic acid (TNBS), to the frog neuromuscular junction in high-magnesium Ringer solution rapidly increased both the amplitude of nerve-evoked end-plate potentials (EPPs) and the frequency of miniature end-plate potentials (MEPPs). These showed a similar initial time course and reached a maximum 3-7 min and about 10 min, respectively, after the start of application of 2 mM-TNBS. Then, the EPP amplitude decreased, while the MEPP frequency maintained its plateau value. The increase in transmitter release and the decrease in EPP amplitude by TNBS may have been due to different modes of action. 2. The distribution of MEPP amplitude was unchanged by TNBS treatment. 3. The carbachol-induced postsynaptic potential and the extracellularly recorded presynaptic action current were not affected by TNBS treatment for up to 30 min, indicating that the change in EPP amplitude produced by TNBS was not due to either a postsynaptic effect or a change in action potential at the presynaptic terminal. 4. The frequency of MEPPs was increased by TNBS application even when Ca2+ was omitted from the external Ringer solution or when a specific calcium channel blocker, synthetic omega-conotoxin, was added. This indicates that Ca2+ inflow to the nerve terminal is not necessary for TNBS action. 5. When a calcium chelator, BAPTA, was loaded into the presynaptic nerve terminal, the facilitation of EPPs by trains of nerve stimuli was scarcely observed. This suggested that the cytosolic free Ca2+ in the presynaptic terminal was buffered by BAPTA. Under this condition, the amplitudes of EPPs were increased by TNBS application to the same extent as in the control without BAPTA, but were accompanied by little facilitation. The MEPP frequency was also increased by TNBS to the same extent as in the control. These results suggest strongly that augmentation of transmitter release by TNBS was not due to an increase in cytosolic Ca2+ concentration. 6. These observations suggest that TNBS might react with specific protein(s) on the outer surface of the presynaptic membrane and accelerate the exocytosis of synaptic vesicles.

Action Potentials↗
PubMed2002

Pregabalin (CI-1008) inhibits the trinitrobenzene sulfonic acid-induced chronic colonic allodynia in the rat.

In human, digestive disorders are often associated with visceral pain. In these pathologies, visceral pain threshold is decreased indicating a visceral hypersensitivity. Pregabalin [CI-1008; S-(+)-3-isobutylgaba] presents antihyperalgesic actions in inflammatory somatic pain models. This study was designed to evaluate 1) the effect of injection of TNBS into the colon on visceral pain threshold, and 2) the antihyperalgesic effect of pregabalin on TNBS-induced chronic colonic allodynia. A significant decrease in the colonic pain threshold was observed in trinitrobenzene sulfonic acid (TNBS)-treated animals (17.8 +/- 1.27 versus 43.4 +/- 1.98 mm Hg). Pregabalin (30-200 mg/kg s.c.) and morphine (0.1-1 mg/kg s.c.) showed a dose-related inhibition of TNBS-induced colonic allodynia. Pregabalin did not inhibit the colonic inflammatory effect of TNBS. In normal conditions (control animals), morphine (0.3 mg/kg s.c.) significantly increased the colonic pain threshold, whereas pregabalin (200 mg/kg s.c.) did not modify the colonic pain threshold. Pregabalin suppressed the TNBS-induced colonic allodynia but did not modify the colonic threshold in normal conditions. The ability of pregabalin to block the chronic colonic allodynia indicates that it is effective in abnormal colonic hypersensitivity, suggesting a possible effect in chronic pain in irritable bowel syndrome.

Analgesics, Opioid↗
PubMed2004

Yersinia pseudotuberculosis anti-inflammatory components reduce trinitrobenzene sulfonic acid-induced colitis in the mouse.

Rectal instillation of trinitrobenzene sulfonic acid (TNBS) induces acute colitis in the mouse. We tested the efficacy of Yersinia pseudotuberculosis anti-inflammatory components in preventing TNBS-triggered colitis. Animals were orally inoculated with virulence-attenuated Yersinia cells (a phoP mutant) prior to TNBS administration. Under these experimental conditions, colonic lesions and tumor necrosis factor alpha mRNA levels were significantly reduced.

Animals↗
PubMed2005

CD40 antisense oligonucleotide inhibition of trinitrobenzene sulphonic acid induced rat colitis.

BACKGROUND: CD154/CD40 interactions play a pivotal role both in humoral and cellular immune responses. Their involvement in the pathogenesis of chronic inflammatory bowel disease (IBD) has been revealed by increased expression of CD40 and CD154 in the inflamed mucosa of patients and the therapeutic effects of anti-CD154 antibodies in experimental colitis. Because of adverse side effects however, the use of such antibodies in patients with IBD may be limited. AIMS: An alternative approach to blocking CD154/CD40 interactions by employing a CD40 antisense oligonucleotide (ODN) was explored. RESULTS: After sequencing of the rat CD40 gene, five antisense ODNs were designed, of which one (rAS3) effectively downregulated CD40 expression in rat vascular smooth muscle cells as well as the subsequent changes in gene expression in response to CD40 stimulation. The therapeutic potency of rAS3 was evaluated in the 2,4,6-trinitrobenzene sulphonic acid (TNBS) induced colitis model of the rat. Single intracolonic injection of a liposomal formulation of rAS3 either prior to or post colitis induction markedly suppressed the inflammatory reaction in these animals monitored both macroscopically and microscopically over one week, while application of a scrambled control ODN had no such effects. Moreover, reverse transcription-polymerase chain reaction analyses revealed reduced expression of vascular cell adhesion molecule 1, interleukin 12 p40, and monocyte chemoatractive protein 1 in the inflamed mucosa, which in turn may have contributed to the decrease in leucocyte infiltration judged by immunohistochemistry. CONCLUSIONS: These results suggest that CD40 antisense ODNs effectively interfere with CD154/CD40 interactions in vivo and, therefore, may provide a novel approach to the treatment of patients with chronic IBD.

Animals↗
PubMed2005

Amelioration of 2,4,6-trinitrobenzene sulphonic acid induced colitis in angiotensinogen gene knockout mice.

BACKGROUND: A number of recent studies have demonstrated a protective effect of renin-angiotensin system (RAS) antagonism against immune mediated diseases such as myocarditis, chronic allograft rejection, and antiglomerular basement membrane nephritis. To our knowledge, there has been no report on the immunological contribution of the RAS in colonic tissue. AIMS: We evaluated the direct effect of angiotensin II (AII) on the pathogenesis of immune mediated colitis using angiotensinogen deficient homozygous (Atg-/-) mice. SUBJECTS: 2,4,6-Trinitrobenzene sulphonic acid (TNBS) colitis was induced in Atg-/- and wild-type (Atg+/+) mice. METHODS: Levels of proinflammatory cytokines in the colon were determined by enzyme linked immunosorbent assay. Histological analysis was performed simultaneously. RESULTS: Although Atg-/- mice developed colitis, the degree was much milder than that in Atg+/+ mice (p<0.05). Colonic cytokine analysis showed that the production of proinflammatory cytokines (interleukin (IL)-1beta, interferon gamma (IFN-gamma)) was impaired in Atg-/- mice. Furthermore, expression of cytokines such as IL-4 and IL-10 in the colon was predominant in Atg-/- compared with Atg+/+ mice after TNBS instillation (p<0.005, p<0.01, respectively). Similarly, subcutaneous infusion of losartan suppressed colitis (p<0.05) and the production of proinflammatory cytokines (IL-1beta, IFN-gamma). These results indicate that the RAS is directly involved in the pathogenesis of TNBS colitis through regulation of proinflammatory and anti-inflammatory cytokines in the colon. CONCLUSIONS: This study revealed that the RAS is involved in the immune system in the colon. Antagonism of the RAS is a potential prophylactic strategy for the treatment of human inflammatory bowel disease.

Angiotensin II Type 1 Receptor Blockers↗
PubMed1997

Prophylactic effect of dietary glutamine supplementation on interleukin 8 and tumour necrosis factor alpha production in trinitrobenzene sulphonic acid induced colitis.

BACKGROUND: It is well established that glutamine supplemented elemental diets result in less severe intestinal damage in experimental colitis. However, few studies have examined the mode of action of glutamine in reducing intestinal damage. AIMS: To examine the effects of glutamine supplemented elemental diets on the potent inflammatory cytokines interleukin 8 (IL-8) and tumour necrosis factor alpha (TNF-alpha) in trinitrobenzene sulphonic acid (TNBS) induced colitis which presents with both acute and chronic features of ulcerative colitis. METHODS: Sprague-Dawley rats were randomised into three dietary groups and fed 20% casein (controls), or 20% casein supplemented with either 2% glutamine (2% Gln) or 4% glutamine (4% Gln). After two weeks they received intracolonic TNBS to induce colitis. RESULTS: Both Gln groups of rats gained more weight than the control group (p < 0.05) which had progressive weight loss. Colon weight, macroscopic, and microscopic damage scores for the Gln groups were lower than in the control group (p < 0.05). IL-8 and TNF-alpha concentrations in inflamed colonic tissues were lower in the Gln groups than in the control group (p < 0.05), and correlated well with disease severity. Bacterial translocation was lower both in incidence (p < 0.05) and in the number of colony forming units (p < 0.05) for the Gln groups, than in the control group. With respect to all indices studied, the 4% Gln group performed better than did the 2% Gln group. CONCLUSION: Prophylactic glutamine supplementation modulates the inflammatory activities of IL-8 and TNF-alpha in TNBS induced colitis.

Analysis of Variance↗
PubMed1999

Role of inducible nitric oxide synthase in trinitrobenzene sulphonic acid induced colitis in mice.

BACKGROUND: Studies using inhibitors of nitric oxide synthase (NOS) to date are inconclusive regarding the role of inducible NOS (iNOS) in intestinal inflammation. AIMS: (1) To examine the role of iNOS in the development of chronic intestinal inflammation; (2) to identify the cellular source(s) of iNOS. METHODS: Colitis was induced by an intrarectal instillation of trinitrobenzene sulphonic acid (TNBS, 60 mg/ml, 30% ethanol), in wild type (control) or iNOS deficient mice. Mice were studied over 14 days; the colons were scored for injury and granulocyte infiltration was quantified. Blood to lumen leakage of (51)Cr-EDTA was measured as a quantitative index of mucosal damage. RESULTS: At 24 and 72 hours, iNOS deficient mice had significantly increased macroscopic inflammation compared with wild type mice. Granulocyte infiltration increased significantly at 24 hours and remained elevated in iNOS deficient mice at 72 hours, but significantly decreased in controls. However, by seven days post-TNBS macroscopic damage, microscopic histology, granulocyte infiltration, and mucosal permeability did not differ between wild type and iNOS deficient mice. A four- to fivefold increase in iNOS mRNA was observed in wild type mice at 72 hours and seven days post-TNBS and was absent in iNOS deficient mice. Immunohistochemistry techniques showed that iNOS expression was predominantly localised in neutrophils, with some staining also in macrophages. CONCLUSIONS: These results suggest that leucocyte derived iNOS ameliorates the early phase, but does not impact on the chronic phase of TNBS induced colitis despite the presence of iNOS.

Acute Disease↗
PubMed2001

Role of T lymphocytes in rat 2,4,6-trinitrobenzene sulphonic acid (TNBS) induced colitis: increased mortality after gammadelta T cell depletion and no effect of alphabeta T cell depletion.

BACKGROUND AND AIM: Indirect evidence suggests that CD4+ T cells have a pathogenic while gammadelta T cells have a protective role in the initiation and perpetuation of inflammatory bowel disease. To define the role of T cell subsets in a rat colitis model (2,4,6-trinitrobenzene sulphonic acid (TNBS)) we analysed colitis severity after effective depletion of T helper cells, alphabeta T cells, or gammadelta T cells. METHODS: T helper cells, alphabeta T cells, or gammadelta T cells were depleted using previously described monoclonal antibodies directed at the CD4 molecule (OX38), the CD2 molecule (OX34, both depleting CD4+ T cells), the alphabeta T cell receptor (R73), and the gammadelta T cell receptor (V65). Depletion was verified by flow cytometry and/or immunohistology. Colitis was induced using intracolonic application of TNBS. RESULTS: Surprisingly, depletion of T helper cells or alphabeta T cells had no influence on survival, macroscopic or microscopic scores, or myeloperoxidase activity following colitis induction. In contrast, depletion of gammadelta T cells resulted in significantly increased mortality (V65: 73%, n=15) compared with controls (30%, n=13; p<0.03). In addition, colitis was histologically more severe in the gammadelta T cell depleted group compared with controls (p<0.05). CONCLUSIONS: T helper cells or alphabeta T cells did not influence the initiation or perpetuation of rat TNBS colitis. In contrast, gammadelta T cells had a protective role in rat TNBS colitis as depletion caused increased mortality.

Animals↗
PubMed2004

Concurrent infection with Schistosoma mansoni attenuates inflammation induced changes in colonic morphology, cytokine levels, and smooth muscle contractility of trinitrobenzene sulphonic acid induced colitis in rats.

BACKGROUND AND AIMS: Crohn's disease, characterised by chronic T helper 1 (Th1) inflammation and dysmotility of the gut, is most prevalent in developed countries. Parasitic infections are most prevalent in developing countries and induce a T helper 2 (Th2) immune response. We hypothesised that this Th2 immune response protects against Th1 gut inflammation. METHODS: The parasite Schistosoma mansoni induces a transient Th2 immune response in the semipermissive rat host. 2,4,6-Trinitrobenzene sulphonic acid (TNBS) induced colitis is an experimental model of Th1-like gut inflammation. The effect of concurrent infection with S mansoni on the course of TNBS induced colitis was assessed using macroscopic and microscopic damage scores, histology, myeloperoxidase (MPO) activity assay, cytokine production assay, and by studying in vitro contractility of longitudinal and circular colonic muscle strips. RESULTS: TNBS induced colitis that spontaneously healed after four weeks. Concurrent infection with S mansoni significantly reduced the duration of TNBS induced colitis to two weeks, as shown by macroscopic and microscopic damage scores and by a faster decrease in colonic MPO activity. TNBS increased colonic interleukin 2 (IL-2) production whereas S mansoni increased splenic IL-4 and IL-2 levels. Contractility of longitudinal and circular muscle strips was maximally inhibited one week after TNBS and normalised after three weeks. After four weeks, longitudinal muscle strip contractility was significantly increased. Concurrent infection with S mansoni normalised longitudinal muscle contractility after one week whereas circular muscle contractility remained inhibited. CONCLUSIONS: Concurrent infection with S mansoni significantly attenuates TNBS induced colitis in the rat. Inflammation induced disturbances in contractility of longitudinal and circular colonic muscle strips may outlast the inflammatory reaction.

Animals↗
PubMed2001

Protective role of heme oxygenase-1 on trinitrobenzene sulfonic acid-induced colitis in rats.

Preliminary studies showed that the inducible form of heme oxygenase (HO-1) was induced and played a protective role in the process of inflammation. The present study investigated the possible role of HO-1 in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in rats. We measured HO-1 activity in TNBS-induced colitis in rats and analyzed the severity of colitis along with altered HO activity by assessing lesion area and myeloperoxidase activity. HO-1 mRNA and protein expressions were determined at different time points after TNBS induction. Free radical production and inducible nitric oxide synthase (iNOS), which participate in oxidative injury, were also assayed. HO activity and HO-1 gene expression increased markedly after TNBS induction. Administration with tin mesoporphyrin (SnMP), a HO inhibitor, potentiated the colonic damage along with a reduction in HO-1 activity. Furthermore, the reduction of HO-1 expression by SnMP also enhanced reactive oxygen species and iNOS expression, both of which were dramatically increased after the TNBS enema. L-Arginine pretreatment further aggravated the injurious action of SnMP. Our results indicate that HO-1 plays a protective role in the colonic damage induced by the TNBS enema, and the preventive effects probably result from decreased free radical production and inhibition of iNOS expression in colonic tissues.

Animals↗
PubMedDate not supplied

Role of endothelins in trinitrobenzene sulfonic acid-induced colitis in rats.

To determine the role of endothelins (ET) on experimental colitis, following intracolonic trinitrobenzene sulfonic acid administration, rats were given orally either bosentan (BS), a nonselective ET receptor antagonist (100 mg/kg in 5% arabic gum), or arabic gum by gavage for 2 or 14 days. Macroscopic damage scores obtained in the vehicle (1.4+/-0.4), acute (4.8+/-0.6) and chronic (3.8+/-0.3) colitis groups were significantly higher than in the control group (0). BS treatment reduced the scores in both acute (3+/- 0.5) and chronic (2.3+/-0.5) colitis groups. Myeloperoxidase (MPO) activities of colonic tissues were elevated in acute and chronic colitis groups (325.1+/-44.9 and 431.8+/-54.6 U/g wet weight) as compared with the control group (73.6+/-11 U/g wet weight). Plasma protein oxidation levels were found to be significantly increased in the chronic colitis group (1,158.1+/-63.4 nmol/ml) compared with the control, ethanol and acute colitis groups (274.3+/-23.1, 490+/-52.2 and 422.2+/-50.5 nmol/ml). BS treatment significantly reduced both the protein oxidation level (375.5+/-46.9 nmol/ml) and MPO activity (167.5+/-35.8 U/g wet weight). The results of the present study suggest the involvement of ETs in the pathogenesis of colonic injury in this animal model of colitis.

Analysis of Variance↗
PubMed2006

Interleukin-6 genetic ablation protects from trinitrobenzene sulfonic acid-induced colitis in mice. Putative effect of antiinflammatory cytokines.

BACKGROUND: Interleukin (IL)-6 is a proinflammatory cytokine implicated in the pathogenesis of inflammatory bowel disease. IL-6 is locally upregulated in inflammatory bowel disease patients and in murine models of experimental colitis. Treatment with anti-IL-6 receptor antibody ameliorates intestinal inflammation. OBJECTIVE: It was the aim of this study to investigate the role of genetic IL-6 deficiency in trinitrobenzene sulfonic acid (TNBS)-mediated colitis, an experimental model inflammation that shares several features with Crohn's disease in humans. METHODS: Acute colitis was induced in wild-type and IL-6-deficient (Il-6(-/-)) mice by intracolonic administration of TNBS. Forty-eight hours after treatment, the local and systemic features of inflammation, i.e. food intake, weight loss, histological markers of colitis, cytokine expression by real-time PCR, food intake and body weight changes, were assessed. RESULTS: In wild-type mice, TNBS administration increased both IL-6 serum levels and local expression of IL-6 by 36 and 9 fold, respectively, compared with control, vehicle-injected mice. Compared with the wild-type mice, the Il-6(-/-) mice had significantly reduced intestinal inflammation as evidenced by epithelial damage, neutrophil infiltration, colon thickness and proinflammatory cytokine expression, following treatment with TNBS. Moreover, baseline levels of the antiinflammatory cytokines IL-10 and tumor growth factor-beta were significantly elevated in Il-6(-/-)compared with the wild-type mice. CONCLUSIONS: Our results demonstrate that Il-6(-/-)are partially protected from the development of TNBS-induced acute experimental colitis, most likely via their significantly elevated baseline levels of antiinflammatory cytokines.

Animals↗
PubMed1998

[Effect of plaunotol on trinitrobenzene sulfonic acid and acetic acid induced colonic lesions in rats].

The aim of this study was to assess the effect of plaunotol, an anti-ulcer agent, on trinitrobenzene sulfonic acid (TNB)- and acetic acid-induced colonic lesions in rats. Plaunotol significantly reduced the severity of colonic mucosal lesions induced by TNB at a dose of 600 mg/kg/day. Moreover, plaunotol, at a dose of 600 mg/kg/day, significantly depressed the myeloperoxidase activity of the lesioned area induced by TNB of the rat colon. In the model of colitis induced by acetic acid, plaunotol reduced the area of lesions dose-dependently and significantly at doses of 60, 200 and 600 mg/kg/day as assessed by macroscopic observation. Microscopic observation showed obvious changes by administration of plaunotol such as reduction of epithelial cell necrosis, decreased mucin production and a decreased infiltration of a large number of neutrophils. In conclusion, plaunotol showed a protective effect against colonic lesion formation induced by TNB and acetic acid in rats. This study suggests the possibility that plaunotol may be effective and useful for treatment of inflammatory bowel disease in humans.

Acetic Acid↗
PubMed2005

Thromboxane A2 up-regulates neutrophil elastase release in Syrian hamsters with trinitrobenzene sulfonic acid-induced colitis.

Neutrophil elastase (NE) is a factor that aggravates colitis. We investigated the influence of thromboxane A2 (TXA2) and leukotriene B4 (LTB4) on NE release in Syrian hamsters with trinitrobenzene sulfonic acid-induced colitis. Colonic specimens with colitis were incubated with U-46619 (a TXA2 analogue) or LTB4 in vitro and NE release was examined. As a result, U-46619 increased NE release, while LTB4 had no effect. The NE release induced by U-46619 was inhibited by a TP-receptor antagonist. To demonstrate that TXA2 caused NE release in vivo as well, while LTB4 did not, colitis animals were treated with nordihydroguaiaretic acid (NDGA), a dual inhibitor of cyclooxygenase/lipoxygenase; and colonic luminal TXB(A)2 and LTB4 levels and NE activity were determined. The TXB(A)2 level was significantly correlated with NE activity, while no correlation was found between LTB4 and NE activity. An inhibitory effect of NDGA on the ulcer area was also observed, and NE activity was significantly correlated with the ulcer area. The suppression of TXA2 production by NDGA may result in the inhibition of NE release so that colonic tissue damage becomes less severe. Regulation of NE release is a new biological action of TXA2 that has not been reported before.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2005

Milk whey culture with Propionibacterium freudenreichii ET-3 is effective on the colitis induced by 2,4,6-trinitrobenzene sulfonic acid in rats.

This study aimed to evaluate whether milk whey culture with Propinibacterium freudenreichii ET-3 (milk whey culture), which has been reported to have Bifidogenic activity, is effective on the colitis induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS) in rats. For the induction of colitis, the colon was clamped and 0.1 M TNBS in 35% ethanol was injected into the luminal side of the clamped portion under pentobarbital anesthesia. From the next day of colitis induction, milk whey culture was administered orally at doses of 1 and 3 g/kg, twice a day for 9 days. On the 10th day, rats were sacrificed and ulcer size was measured. Milk whey culture significantly accelerated the healing of the colitis in a dose-dependent manner, but culture medium did not. To clarify the active substance, the effects of propionic acid and acetic acid contained in milk whey culture was tested. Sodium propionate significantly accelerated the healing of TNBS-induced colitis, but sodium acetate did not. The above results show that milk whey culture may become a useful prebiotic for the therapy of inflammatory bowel disease and that propionic acid may be one of the active substances contained in milk whey culture.

Acetic Acid↗
PubMed2005

An improved and reliable method for the induction of colitis in rats using 2,4,6-trinitrobenzene sulfonic acid.

We performed this study to develop a reliable method for inducing colitis in rats using 2,4,6-trinitrobenzene sulfonic acid (TNBS) to reduce the variation in ulcer size. A pair of ring forceps was used to clamp the colon and 0.1 M TNBS in ethanol was injected into the luminal side of the clamped portion. This method resulted in a small coefficient of variation of the ulcer index. A significant linearity was observed by plotting ulcer size against days after ulcer induction in both logarithm scales. These findings show that this technique is simple and reliable and that ulcers heal linearly.

Animals↗
PubMed2004

Dietary resistant starch alters the characteristics of colonic mucosa and exerts a protective effect on trinitrobenzene sulfonic acid-induced colitis in rats.

The protective effect of a dietary high-amylose cornstarch (HAS) against trinitrobenzene sulfonic acid (TNBS)-induced colitis was examined in rats. Rats were fed a HAS-free basal diet or, a 15% or 30% HAS supplemented diet for 10 d, and then received intracolonic TNBS to induce colitis and fed the respective diets for a further 8 d. HAS ingestion significantly protected colonic injuries as evidenced by lower colonic myeloperoxidase activity. Rats fed the HAS diet showed greater cecal short-chain fatty acid (SCFA) production than those fed the basal diet. Further, just before TNBS administration, HAS ingestion dose-dependently increased fecal and cecal mucin contents, and protein and nucleic acid contents in the colonic mucosa. HAS ingestion also reduced colonic permeability. The protective effect of HAS ingestion on TNBS-induced colitis is perhaps exerted through alterations in colonic mucosa, possibly due to cecal SCFA production.

Animals↗