Bowel Disease In Rats Research Articles

Therapeutic potentials of mesenchymal stem cells in the treatment of inflammatory bowel disease in rats.

Interleukin-1beta (IL-1β) and interleukin-17A (IL-17A) have strong pro-inflammatory activities that are involved in inflammatory bowel diseases (IBDs). Mesenchymal stem cell (MSC) therapy is considered a promising treatment for IBD. This study was performed to understand the role of rat Nlrp3 inflammasome, Hmgb1, and pro-inflammatory cytokines (IL-1β and IL-17a) in the pathogenesis of IBD. Also, to evaluate the role of human umbilical cord blood-MSCs (hUCB-MSCs) in the management of IBD. The rats were in four groups: normal controls, indomethacin-induced IBD group, indomethacin-induced IBD rats that received phosphate-buffered saline (PBS), and the IBD group that received hUCB-MSCs as a treatment. The messenger RNA (mRNA) expression levels of rat Nlrp3, Hmgb1, IL-1β, and IL-17a were evaluated by quantitative real-time polymerase chain reaction.Histopathological examination of the small intestinal tissues of the studied rats was performed. There was a significant upregulation of the rat Nlrp3, IL-1β, IL-17a mRNA expression (p < 0.001 for the three parameters), and Hmgb1 (p < 0.05) in the untreated IBD group compared to the normal control group. In the MSC-treated group, IL-1β, IL-17a, and rat Nlrp3 mRNA expression significantly decreased compared to both the untreated IBD group and PBS group (p < 0.05 for all). hUCB-MSCs ameliorated IBD in rats by downregulating the pro-inflammatory cytokines (IL-1β and IL-17a) and other inflammatory mediators such as Hmgb1 and rat Nlrp3.

Glepaglutide, a novel glucagon-like peptide-2 agonist, has anti-inflammatory and mucosal regenerative effects in an experimental model of inflammatory bowel disease in rats

BackgroundGlucagon-like peptide-2 (GLP-2) enhances intestinal repair and attenuates inflammation in preclinical inflammatory bowel disease (IBD) models, making GLP-2 analogues attractive candidates for IBD therapy. Glepaglutide is a long-acting GLP-2 receptor agonist in clinical development for treatment of short bowel syndrome. Here, we investigated if glepaglutide is therapeutically beneficial in rats with small intestinal inflammation.MethodsSmall intestinal inflammation was induced with indomethacin in naive Wistar rats, followed by glepaglutide administration at different disease stages. Glepaglutide was administered in co-treatment and post-treatment regimens. Small intestinal length and concentrations of inflammatory markers α-1-acid glycoprotein and myeloperoxidase were used to assess anti-inflammatory effects. Small intestinal mass was evaluated to determine intestinotrophic effects.ResultsGlepaglutide co- and post-treatment significantly reduced severity of small intestinal inflammation, evidenced by reversed small intestinal shortening and decreased α-1-acid glycoprotein and/or myeloperoxidase concentration(s). Co- and post-treatment with glepaglutide also significantly increased small intestinal mass, indicating intestinal regenerative effects. Similar effects were observed in naive rats after glepaglutide treatment.ConclusionGlepaglutide has anti-inflammatory and intestinotrophic effects without the need for pre-treatment in a rat model of small intestinal inflammation. Thus, glepaglutide is of potential clinical interest for patients with IBD.

Dark-purple rice extract modulates gut microbiota composition in acetic acid- and indomethacin-induced inflammatory bowel disease in rats.

Ulcerative colitis (UC) and Crohn's disease (CD) are two major forms of inflammatory bowel disease (IBD). The disease has been linked with gut microbiota dysbiosis in which the balance of commensal communities is disrupted. Accumulating evidence demonstrates that treatment with biologically active compounds can modulate gut microbiota composition in animal models. Our previous work has also shown the beneficial effect of Luem Pua (LP) rice extract, which is rich in anthocyanins, on inflammation. However, its effect on gut microbiota is yet to be explored. In this study, we profiled fecal microbiota of acetic acid (AA)-induced UC and indomethacin (ID)-induced CD rat models with and without pretreatment with LP rice extract by 16S rRNA gene sequencing. The results showed that gut microbiota communities of rats were altered by both AA-induced UC and ID-induced CD. The relative abundances of beneficial bacteria, especially the Lachnospiraceae NK4A136 group and Lactobacillus, were decreased in the AA-induced UC model, while some opportunistic pathogens (Bacteroides, Escherichia/Shigella, Fusobacterium, and Veillonella) were raised by ID-induced CD. Interestingly, pretreatment with LP rice extract before AA-inducing UC in rats increased the proportion of the butyrate-producing bacteria (Lachnospiraceae NK4A136 group). The abundances of these beneficial bacteria and other SCFA-producing bacteria were unaffected by the indomethacin treatment with LP. Overall, our study revealed different impacts of AA-induced UC and ID-induced CD on changes in community composition and hinted at how LP may protect against UC by modifying the gut microbiota.

Oral administration of pasteurized probiotic fermented milk alleviates dextran sulfate sodium-induced inflammatory bowel disease in rats

• DSS induction increased inflammatory response and disturbed gut microbiota in IBD rats. • Pasteurized probiotic fermented milk significantly reduced serum pro-inflammatory TNF-α and IL-6 level. • Pasteurized probiotic fermented milk attenuated the inflammatory injury of colon tissue. • Pasteurized probiotic fermented milk restored the host gut microbiota disturbed by DSS. The pathogenesis of inflammatory bowel disease (IBD) is closely related to inflammatory damage and gut dysbiosis. Administering fermented milk may serve as a dietary intervention strategy of delivering bioactive substrates to consumers. This work aimed to investigate the mitigating effects of pasteurized probiotic fermented milk on dextran sulfate sodium (DSS)-induced IBD in rats. Our results showed that intragastric gavage of pasteurized probiotic fermented milk could significantly lower DAI scores, alleviate colon damage, and decrease serum tumor necrosis factor-α and interleukin-6 levels. Additionally, pasteurized probiotic fermented milk administration improved the intestinal microbial Richness index, accompanied by significant increases in beneficial bacteria and reduction in species related to host inflammation. The gut functional metagenome also shifted with pasteurized probiotic fermented milk intervention, showing significant enrichment in biosynthesis pathways of amino acids, nucleotides, and vitamins. In conclusion, ingesting pasteurized probiotic fermented milk alleviated IBD by reducing inflammatory response and restoring the gut microbiota.

In vivo assessment of inflammatory bowel disease in rats with ultrahigh-resolution colonoscopic OCT.

A technology capable of high-resolution, label-free imaging of subtle pathology in vivo during colonoscopy is imperative for the early detection of disease and the performance of accurate biopsies. While colonoscopic OCT has been developed to visualize colonic microstructures beyond the mucosal surface, its clinical potential remains limited by sub-optimal resolution (∼6.5 µm in tissue), inadequate imaging contrast, and a lack of high-resolution OCT criteria for lesion detection. In this study, we developed an ultrahigh-resolution (UHR) colonoscopic OCT and evaluated its ability to volumetrically visualize and identify the pathological features of inflammatory bowel disease (IBD) in a rat model. Owing to its improved resolution (∼1.7 µm in tissue) and enhanced contrast, UHR colonoscopic OCT can accurately delineate fine colonic microstructures and identify the pathophysiological characteristics of IBD in vivo. By using a quantitative optical attenuation map, UHR colonoscopic OCT is able to differentiate diseased tissue (such as crypt distortion and microabscess) from normal colonic mucosa over a large field of view in vivo. Our results suggest the clinical potential of UHR colonoscopic OCT for in vivo assessment of IBD pathology.

Optimization and Validation of Polyherbal Formulation by Applying Boxbehnken Design for the Treatment of Inflammatory Bowel Disease in Experimental Animals

Background: The use of herbal medicine in inflammatory bowel disease (IBD) has increased significantly. Allopathic treatment of IBD leads to several side effects; therefore, the use of the herbal formulation is promising. Aegle Marmelos, Bombax malabericum, and Hollarrhena antidysentrica plants have been used to treat IBD. Objective: This study aimed to evaluate a designed polyherbal formulation in experimentally induced inflammatory bowel disease in rats and validate a mathematical model derived by Box-Behnken experimental design for optimized polyherbal formulation for the treatment of IBD in experimental rats by checkpoint analysis. Method: Three-level Box-Behnken design was selected to optimize the dose. Polyherbal formulation that consisted of plant extracts of Aegle Marmelos (X1), Bombax malabericum (X2), and Hollarrhena antidysentrica (X3) in different ratios was selected as an independent variable. Polynomial equations were established based on analysis of variance (ANOVA). To validate the chosen polynomial equation, checkpoint analyses were performed. The percentage of predictive error is presented. Results: ANOVA reveals that X2 plant does not have any significant impact on the response surface. The checkpoint batch showed the experimental values of CMDI and Disease activity index (DAI) as 1.33 and 0.66, respectively. It is worthwhile to note that the observed values were quite close to the calculated values of CMDI. A little difference in the value of DAI may be attributed to the inherent variation observed in animal studies. Conclusion: From this study, it was concluded that a dose of 100 mg/kg of Aegle marmelos, a dose of 300 mg/kg of Bombax malabericum, and a dose of 200 mg/kg of Holarrhena antidysentrica will be effective in IBD patients.

Effect of Aminosteroid U74389G in a Model of Inflammatory Bowel Disease in Rats

Summary Lazaroid U-74389G is a synthetic 21-aminosteroid with free radical-scavenging and anti-inflammatory effects. This study was designed to evaluate the anti-inflammatory activity of U-74389G on experimental 2,4-dinitrobenzene sulfonic acid hydrate (DNBS)-induced colitis in Wistar rats. Five experimental groups were formed: a sham control group, a control group, treated with 0.25 ml of 50% ethanol intrarectally (n=8), a group treated with DNBS (30 mg in 0.25 ml of 50% ethanol administered intrarectally, (n=8), a group treated with DNBS and U-74389G at a daily dose of 15 mg/kg i.p. (n=8), and a group treated with DNBS and sulfasalazine, orally, at a dose of 300 mg/kg. During the experiment, the bodyweight of the rats, food intake, stool consistency, and presence of blood in the stool were recorded as markers of clinical condition. On day 6, colonic tissues were excised and scored for macroscopic and histological damage. Blood samples were taken to measure levels of cytokines by ELISA methods. DNBS decreased significantly body weight (from 237.00±2.52 g to 212.50±6.25 g, p=0.04). The rats treated with U-74389G showed greater food intake and weight gain. U-74389G reduced ulceration index: the U-74389G score was 1.25±0.25, and the DNBS score –3.87±0.61; p&lt;0.05. All other macroscopic parametersassessed were significantly improved in rats treated with U-74389G. The levels of inflammatory cytokines IL-1, IL-6, and TNF-α, were significantly lower than those of the DNBS group, while U-74389G significantly elevated the level of anti-inflammatory IL-10. These findings indicate that U-74389G significantly inhibits colonic inflammatory damages in a rat model of inflammatory bowel disease.

Linagliptin mitigates experimental inflammatory bowel disease in rats by targeting inflammatory and redox signaling

AimsDipeptidyl peptidase-4 (DPP-4) has been involved in the pathogenesis of inflammatory bowel diseases (IBD), yet the underlying mechanisms remain inconclusive. The present study aimed to investigate the potential of linagliptin, a potent/selective DPP-4 inhibitor with marked anti-inflammatory actions, to attenuate trinitrobenzene sulfonic acid (TNBS)-evoked colitis in rats; an experimental model of IBD, and the implicated molecular mechanisms. This may add to the clinical utility of linagliptin for the management of patients with coexisting IBD and diabetes mellitus. Notably, no former studies have linked JAK2/STAT3, HMGB1/NF-κB, and Nrf2/HO-1 signaling in TNBS-evoked colitis. Materials and methodsWestern blotting and ELISA were used to determine the levels of target signals. Key findingsAdministration of linagliptin (1.5 mg/kg; p.o.) mitigated the colitis severity via diminishing the disease activity index, colon weight/length ratio, and macroscopic scores. Linagliptin also lowered the colonic histologic scores and leukocyte invasion. Notably, linagliptin inhibited the colonic DPP-4 activity and upregulated the expression of intestinotrophic GLP-2 without incurring hypoglycemia in animals. Linagliptin curbed inflammation through the suppression of colonic IL-6, TNF-α, and myeloperoxidase and upregulation of IL-10. It also inhibited the IL-6/JAK2/STAT3 pathway via downregulating p-JAK2/JAK2 and p-STAT3/STAT3 protein expression and HMGB1/RAGE/NF-κB cascade through lowering HMGB1, RAGE, and p-NF-κB p65/NF-κB p65 protein expression. In the context of mucosal oxidative stress, linagliptin diminished lipid peroxides and augmented GSH, GPx, and total antioxidant capacity. It also activated Nrf2/HO-1 pathway via upregulating Nrf2 and HO-1 protein expression. SignificanceLinagliptin shows a promise for the management of IBD via targeting IL-6/JAK2/STAT3, HMGB1/RAGE/NF-κB, and Nrf2/HO-1 pathways.

Activation of autophagy and suppression of apoptosis by dapagliflozin attenuates experimental inflammatory bowel disease in rats: Targeting AMPK/mTOR, HMGB1/RAGE and Nrf2/HO-1 pathways

Dapagliflozin, a selective sodium-glucose co-transporter 2 (SGLT2) inhibitor, has featured marked anti-inflammatory effects in murine models of myocardial infarction, renal injury, and neuroinflammation. Yet, its potential impact on the pathogenesis of inflammatory bowel diseases (IBD) has not been previously investigated. The presented study aimed to explore the prospect of dapagliflozin to mitigate 2,4,6 trinitrobenzene sulfonic acid (TNBS)-induced rat colitis model which recapitulates several features of the human IBD. The molecular mechanisms pertaining to the dynamic balance between autophagy/apoptosis and colon injury were delineated, particularly, AMPK/mTOR, HMGB1/RAGE/NF-κB and Nrf2/HO-1 pathways. The colon tissues were examined using immunoblotting, ELISA, and histopathology. Dapagliflozin (0.1, 1 and 5 mg/kg; p.o.) dose-dependently mitigated colitis severity as manifested by suppression of the disease activity scores, macroscopic damage scores, colon weight/length ratio, histopathologic perturbations, and inflammatory markers. More important, dapagliflozin enhanced colonic autophagy via upregulating Beclin 1 and downregulating p62 SQSTM1 protein expression. In this context, dapagliflozin activated the AMPK/mTOR pathway by increasing the p-AMPK/AMPK and lowering the p-mTOR/mTOR ratios, thereby, favoring autophagy. Moreover, dapagliflozin dampened the colonic apoptosis via lowering the caspase-3 activity, cleaved caspase-3 expression, and Bax/Bcl-2 ratio. Furthermore, dapagliflozin attenuated the HMGB1/RAGE/NF-κB pathway via lowering HMGB1, RAGE, and p-NF-κBp65 protein expression. Regarding oxidative stress, dapagliflozin lowered the oxidative stress markers and augmented the Nrf2/HO-1 pathway. Together, the present study reveals, for the first time, the ameliorative effect of dapagliflozin against experimental colitis via augmenting colonic autophagy and curbing apoptosis through activation of AMPK/mTOR and Nrf2/HO-1 pathways and suppression of HMGB1/RAGE/NF-κB cascade.

Effects of Vitamin D3 on Inflammatory Bowel Disease in Rats via the Toll-Like Receptor 4/ Myeloid Differentiation Primary Response 88/ Nuclear Factor Kappa Light Chain Enhancer of Activated B Cells Signaling Pathway

To assess the ameliorating effects of vitamin D3 on inflammatory bowel disease in rats via the Toll-like receptor 4/myeloid differential factor 88/nuclear factor kappa B signaling pathway. Thirty two rats were randomly assigned into Control group, model group (Vehicle group), low-concentration vitamin D3 group (vitamin D3 low group) and high-concentration vitamin D3 group (vitamin D3 high group). The model of inflammatory bowel disease was constructed using 3 % dextran sodium sulfate and given different concentrations of vitamin D3. Disease activity index score was calculated, colon tissues were pathologically scored by hematoxylin-eosin staining, and the mRNA expression levels of Toll-like receptor 4/myeloid differential factor 88/nuclear factor kappa B were measured by quantitative reverse transcriptionpolymerase chain reaction. The expression levels of serum tumor necrosis factor-α, pro-inflammatory factors interleukin 1β and interleukin 6, as well as anti-inflammatory factor interleukin 10 were detected through enzyme-linked immunosorbent assay. The disease activity index score, mRNA expression levels of Toll-like receptor 4/myeloid differential factor 88/nuclear factor kappa B and expression levels of tumor necrosis factor-α, interleukin 1β and interleukin 6 were significantly higher in Vehicle group than those in Control group, while the expression level of interleukin-10 was lower in Vehicle group (p<0.05). After intervention with vitamin D3, vitamin D3 low group and vitamin D3 high group had significantly decreased disease activity index score, messenger RNA expression levels of Toll-like receptor 4/myeloid differential factor 88/nuclear factor kappa B and expression levels of tumor necrosis factor-α, interleukin 1β and interleukin 6, increased interleukin-10 expression level, and relieved damage of colon tissues compared with Vehicle group (p<0.05). Vitamin D3 ameliorates intestinal injury and colonic inflammation in inflammatory bowel disease rats by suppressing the Toll-like receptor 4/myeloid differential factor 88/ nuclear factor kappa B signaling pathway and decreasing the expression of downstream pro-inflammatory factors.

The healing effects of prp and thymoquinone on dss induced inflammatory bowel disease in rats

Aim: Crohn's disease and ulcerative colitis are included in inflammatory bowel disease (IBD). The study aimed to compare the healing effects of two promising therapeutic agents: Platelet Rich-Plasma and Thymoquinone (TQ) on DSS induced IBD.Materials and Methods: The animals were divided into three groups as IBD (n=10), PRP treatment (n=10) and TQ treatment (n=10). Experimental IBD was initiated through the oral intake of 5% Dextran Sodium Sulfate (DSS) in drinking water. PRP (0.5 cc) and thymoquinone dissolved in distilled water (100mg/kg) were daily administered rectally to PRP treated group animals for seven days. All animals were sacrificed and rectal tissue calprotectin, lactoferrin and hydroxyproline levels were assessed on the seventh day. Total antioxidant status (TAS), total oxidant status (TOS) and oxidative stress index (OSI) levels were statistically compared.Results: Rectal tissue calprotectin, lactoferrin and hydroxyproline levels were higher in the IBD group (p<0.001, p<0.001 and p<0.001, respectively). TQ treated group animals had lower rectal tissue lactoferrin levels (p<0.011) and TOS and OSI levels (p=0.001 and p=0.001, respectively) than PRP group animals and also the highest antioxidant capacity.Conclusion: Calprotectin, lactoferrin, and hydroxyproline levels are valuable markers in the presence of IBD and response to treatment. Oxidative stress is an important problem that cannot be avoided in unattended cases. Our experimental IBD model found TQ treatment to be more effective in healing than PRP treatment.

Cyanidin 3-glucoside from Queen Garnet plums and purple carrots attenuates DSS-induced inflammatory bowel disease in rats

We have investigated whether dextran sodium sulphate (DSS)-induced inflammatory bowel disease (IBD) in rats can be ameliorated by intervention with cyanidin 3-glucoside (C3G). Rats were given either normal water (C) or 0.5% DSS (D) in drinking water for 12 weeks. C3G 8 mg/kg/day as Queen Garnet plum (Q) juice, purple carrot (P) juice or pure compound was added in food for final 6 weeks to C rats to give CQ, CP and CC groups, and to D rats to give DQ, DP and DC groups. No symptoms of IBD were observed in C, CQ, CP or CC rats. D rats had bloody diarrhoea, ileal and colonic mucosal atrophy, and inflammation. Compared to D rats, DQ, DP and DC rats showed improved stool consistency (P < 0.0001) and bleeding (P < 0.0001), reduced ileum (P < 0.0001) and colon inflammation (P < 0.0001), with no changes in gut microbiota. Thus, supplementation with C3G-containing foods may ameliorate the symptoms of IBD.

Evaluation of the Activity of Leea Indica Merrill in Inflammatory Bowel Disease using Experimental Models

Leea indica is traditionally well-known for its versatile uses. The present study was carried out to evaluate the protective effect of methanolic extract of Leea Indica on DNBS (2, 4 dinitrobenzene sulfonic acid) induced inflammatory bowel disease in rats. Adult Wistar rats of either sex weighing 150-200 g were selected. Thirty animals were randomly divided into 5 groups each consisting of 6 animals. The period of experiment was of 12 days. Animals of Group I, Group-III, Group-IV &amp; Group-V were given water, methanolic extract of Leea indica (200mg/kg &amp; 400mg/kg) and sulfasalazine (360 mg/kg body weight) respectively once a day orally for 1st to 7th days. On 8th day of the study, DNBS solution (30 mg dissolved in 0.25 ml of 50% ethanol) was administered intrarectally to induce IBD in animals of Group-II to V, on same day &amp; no treatment was given. Then from 9th to 11th day, they were again given treatment. On 12th day, blood was collected from all animals and sacrificed and dissected to isolate colon. Finally, macroscopic, microscopic and biochemical studies were carried out. At all the two doses, the methanolic extract of Leea Indica showed significant anti-inflammatory activity in experimental models. Results obtained in this study substantiate the anti-inflammatory effect of methanolic extract of Leea Indica roots.

Ameliorative effect of chromium-d-phenylalanine complex on indomethacin-induced inflammatory bowel disease in rats.

Present study was designed to evaluate the effect of chromium-d-phenylalanine complex (Cr (d-phe)3) on indomethacin-induced inflammatory bowel disease (IBD) in rats. Adult Wistar rats were pretreated with vehicle/Cr (d-phe)3 (30, 60 and 90μg/kg, p.o.) for 11days. On day 8 and 9, after one h of the above mentioned treatment, indomethacin (7.5mg/kg/day,s.c.) was administered to induce IBD. On day 12, blood samples were collected from animals for lactate dehydrogenase (LDH) estimation and ileum was isolated for macroscopic scoring, biochemical estimation (lipid peroxidation, reduced glutathione and myeloperoxidase activity) and histopathological study. Administration of indomethacin significantly altered the serum LDH, macroscopic and microscopic appearance and biochemical parameters in ileum tissue. Cr (d-phe)3, at all the tested doses, caused a significant reversal of changes induced by indomethacin. Present study demonstrates the protective effect of Cr (d-phe)3 against indomethacin-induced IBD in rats. The observed protective effect might be attributed to the antioxidant and anti-inflammatory properties of Cr (d-phe)3.

Histological and immunohistochemical effects of L-arginine and silymarin on TNBS-induced inflammatory bowel disease in rats.

Inflammatory bowel disease (IBD) is a chronic disease that affects quality of life. Various mediators are involved in IBD pathogenesis including inducible nitric oxide synthase (iNOS), nuclear factor kappa B (NF-κB), cytochrome c, heat shock protein 70 (HSP70) and tumor necrosis factor (TNF)-α. L-Arginine (L-Arg) can be depleted in IBD, and silymarin inhibits neutrophil infiltration, NF-κB, and TNF-α, which have crucial roles in inducing IBD. This study aimed to investigate whether silymarin and L-Arg supplementation decreases IBD progression in trinitrobenzine-sulfonic acid (TNBS)-induced colitis. Fifty adult male albino rats were randomized into five groups (10 animals per group): Group I rats orally received 100 mg silymarin/kg body weight once daily; Group II rats orally received 2 mg L-Arg/100 g body weight in 5 mL distilled water once daily; Group III rats rectally received 0.85 mL TNBS in 50% ethanol to induce colitis; Group IV rats were treated similar to group III and, on recovery from anesthesia, received silymarin as described for group I; and Group V rats were treated similar to group III and, on recovery from anesthesia, received L-Arg as described for group II. On day 7, the rats were anesthetized, and blood samples were collected to determine the serum concentrations of TNF-α. Laparotomy and total colectomy were performed for macroscopic, histological, and immunohistochemical investigations. The results showed that silymarin and L-Arg macroscopically and microscopically ameliorated TNBS-induced colitis; significantly decreased the serum levels of TNF-α; inhibited the colonic expression of iNOS, NF-κB, and cytochrome c; and increased expression of HSP70. Our results suggest that these complementary medicines could be used to supplement current treatments for IBD.

Effect of turmeric on colon histology, body weight, ulcer, IL-23, MPO and glutathione in acetic-acid-induced inflammatory bowel disease in rats.

BackgroundThis study investigates the protective effects of turmeric (Curcuma longa, CL) on acetic acid-induced colitis in rats.MethodInflammatory bowel disease (IBD) was induced in male Wistar rats by intra-rectal administration of 1 ml of 4 % acetic acid at 8 cm proximal to the anus for 30 s. Curcuma longa (CL) powder, (1, 10, or 100 mg/kg/day) was administered for either 3 days before or after IBD for 7 days. The body weight, macroscopic and microscopic analysis of the colon of CL-treated IBD rats and that of control rats (no IBD, no CL) were performed on 0 day, 2, 4 and 7th day. Myeloperoxidase (MPO), IL-23 and glutathione levels in control, untreated and treated rats were measured by ELISA.ResultsCL significantly (P < 0.05) improved IBD-induced reduction in mean body weight and mean macroscopic ulcer score. Administration of CL also significantly (P < 0.01) reduced the mean microscopic ulcer score when compared to untreated IBD control. Intake of CL by rats resulted in a significant (P < 0.05) increase in the mean serum glutathione level compared to untreated control. CL reduced both MPO and IL-23 levels in the colonic mucosa of the rat.ConclusionCL improved body weight gain, mean macroscopic and microscopic ulcer scores in the colon of rats suffering from acetic acid-induced IBD. CL reduced both MPO and IL-23 in the mucosa of the colon. The increase in the mean serum glutathione level may help in the reduction of oxidative stress associated with IBD.

“Effect of Rosiglitazone alone and in combination with Sulfasalazine in experimentally induced inflammatory bowel disease in rats”

Background: Inflammatory bowel disease (IBD) is an idiopathic, chronic inflammatory condition, which affects the gastrointestinal tract and has no curative treatment. The present study aimed to investigate the effect of different doses of Rosiglitazone alone and in combination with sulfasalazine in AA (acetic acid)-induced inflammatory bowel disease (IBD) in rats. Methods: A total of 36 animals were included in the study. Animals were divided into five groups (n = 6): group I - control (normal saline), group II-AA+ normal saline, group III-Sulfasalazine(360mg/kg) +AA, group IV A - Rosiglitazone (1 mg/kg), group IV B- Rosiglitazone 5 mg/kg + AA, group V - Rosiglitazone 5 mg/kg + Sulfasalazine (360 mg/kg) +AA. Group IV was divided into two subgroups, namely IVA and IVB, on the basis of different doses of Rosiglitazone used. After completion of one week of treatment, rats were sacrificed under ether anesthesia for assessment of intestinal inflammation using parameters namely colon weight change, macroscopic and histopathological evaluation. Results: There was a decrease in colonic weight, macroscopic scores and microscopic scores in groups treated with Rosiglitazone at a dose of 5 mg/kg i.e. high dose given alone and in combination with sulfasalazine .Combination treatment was more effective when compared to single drug treatment. Conclusion: The present study indicates the efficacy of Rosiglitazone in Acetic acid-induced IBD. The effects are more pronounced at higher dose i.e., 5 mg/kg. Combination of Rosiglitazone and Sulfasalazine has shown greater efficacy than single drug treatment. Keywords: Inflammatory bowel disease, Rosiglitazone, Colon weight change, Macroscopic evaluation, Histopathological evaluation

Comparative evaluation of different doses of ciprofloxacin alone and in combination with sulfasalazine in experimentally induced inflammatory bowel disease in rats

Background: Inflammatory bowel disease (IBD) is an idiopathic, chronic inflammatory condition, which affects the gastrointestinal tract and has no curative treatment. The present study aimed to investigate the effect of different doses of ciprofloxacin alone and in combination with sulfasalazine in AA (acetic acid)-induced inflammatory bowel disease (IBD) in rats. Methods: A total of 36 animals were included in the study. Animals were divided into five groups (n = 6): group I - control (normal saline), group II-AA+ normal saline, group III-sulfasalazine(360mg/kg) +AA, group IV A - ciprofloxacin (50 mg/kg), group IV B- ciprofloxacin 100 mg/kg + AA, group V - ciprofloxacin 100 mg/kg + sulfasalazine (360 mg/kg) +AA. Group IV was divided into two subgroups, namely IVA and IVB, on the basis of different doses of ciprofloxacin used. After completion of two weeks of treatment, rats were sacrificed under ether anaesthesia for assessment of intestinal inflammation using parameters namely colon weight change, macroscopic and histopathological evaluation. Results: There was a decrease in colonic weight, macroscopic scores and microscopic scores in groups treated with ciprofloxacin at a dose of 100 mg/kg i.e. high dose given alone and in combination with sulfasalazine. Combination treatment was more effective when compared to single drug treatment. Conclusions: The present study indicates the efficacy of ciprofloxacin in acetic acid-induced IBD. The effects are more pronounced at higher dose i.e., 100 mg/kg. Combination of ciprofloxacin and sulfasalazine has shown greater efficacy than single drug treatment.

Anti-inflammatory Activity of Emu Oil in Indomethacin Induced Inflammatory Bowel Disease in Rats

Inflammatory bowel disease is a chronic condition affecting human and animal species. The present study was taken up with the objective to test an animal product, emu oil against inflammatory bowel disease and to evaluate its activity in comparison to aloe vera (plant product) alone and in combination with emu oil. Experiment was performed in six groups containing 6 rats each. Rats were pre-treated for five consecutive days with sulfasalazine [100 mg/kg], aloe vera [400 mg/kg], emu oil [10 ml/kg] and the combination of aloe vera and emu oil to groups III, IV, V and VI respectively. The condition was induced using two consecutive subcutaneous injection of indomethacin [10 mg/kg] on day 4 and 5 in all groups except group I (control). Rats were sacrificed on day 8 and samples were collected for further analysis. Macroscopic lesions include ulceration [pin point to linear], perforation and necrotic epithelium in caecum. Microscopically, there was ulceration [loss of epithelium] and increased cellular infiltration. Emu oil was analysed through Gas chromatography–Mass spectrometry for fatty acid profiling and was found to contain mixture of unsaturated and saturated fatty acids. This was evident through the analysis of inflammatory and oxidative stress parameters of group V when compared to groups III and IV. However, the combination of aloe vera and emu oil showed better activity than all other groups. Hence it was concluded that emu oil might be attempted to treat the inflammatory conditions of gastro-intestinal tract as a part of alternative medicine.

Evaluation of anti-inflammatory activity of Oxalis corniculata in experimentally induced inflammatory bowel disease in rats

Background: Oxalis corniculata is traditionally well-known for its versatile uses. The present study was carried out to evaluate the anti-inflammatory activity of the ethanolic extract of O. corniculata (EEOC) leaves in experimentally induced inflammatory bowel disease in rats. Methods: Rats were treated with the extract for 7 days following which acetic acid was used to induce colitis. Animals were euthanized, 24 hrs after induction of colitis and colon was removed and assessed for macroscopic injury, as well as also processed for histopathological examination. Sulfasalazine 360 mg/kg was used as the standard drug. The extract was used in 200 mg/kg, 300 mg/kg and 400 mg/kg doses. Results: At all the three doses, the EEOC showed significant (p