scholarly journals Intestinal Anti-Inflammatory Activity of the Aqueous Extract from Ipomoea asarifolia in DNBS-Induced Colitis in Rats

2018 ◽  
Vol 19 (12) ◽  
pp. 4016 ◽  
Author(s):  
Valéria da Silva ◽  
Aurigena de Araújo ◽  
Daline Araújo ◽  
Maíra Lima ◽  
Roseane Vasconcelos ◽  
...  
Keyword(s):  
Protective Effect ◽  
Aqueous Extract ◽  
Intestinal Inflammation ◽  
Activity Index ◽  
Immunohistochemical Analysis ◽  
Histological Evaluation ◽  
Myeloperoxidase Activity ◽  
Down Regulation ◽  
Anti Inflammatory ◽  
Ipomoea Asarifolia

Inflammatory bowel disease is triggered by an uncontrolled immune response associated with genetic, environmental, and intestinal microbiota imbalance. Ipomoea asarifolia (IA), popularly known as “salsa” or “brave salsa”, belongs to the Convolvulaceae family. The aim of this approach was to study the preventive effect of IA aqueous extract in 2,4-dinitrobenzene sulfonic acid (DNBS)-induced colitis in rats. Rats pretreated with IA extract or sulfasalazine (SSZ) received intracolonic instillation of DNBS in 50% ethanol (v/v). IA extract presented a protective effect against intestinal inflammation, with improvement in the disease activity index and macroscopic damage. IA or SSZ significantly reduced myeloperoxidase activity, and also down-regulation of the gene expression of JNK1, NF-κβ-p65, STAT3, and decreased levels of TNFα, IL-1β, and increased IL-10, associated with a significant improvement of oxidative stress, in addition to a reduction in MDA and an increase of glutathione in colonic tissue. The protective effect of the extract was also confirmed in histological evaluation, showing preservation of the colonic cytoarchitecture. Immunohistochemical analysis revealed down-regulation of NF-κβ-p65, iNOS, IL-17, and up-regulation of SOCs-1 and MUC-2. IA extract presents antioxidant and anti-inflammatory intestinal properties, and proved to be a potential application for preventing damage induced by DNBS.

scholarly journals Preventative oral methylthioadenosine is anti-inflammatory and reduces DSS-induced colitis in mice

2012 ◽  
Vol 303 (1) ◽  
pp. G71-G82 ◽  
Author(s):  
Nancy M. Benight ◽  
Barbara Stoll ◽  
Juan C. Marini ◽  
Douglas G. Burrin
Keyword(s):  
Time Course ◽  
Intestinal Inflammation ◽  
Tissue Injury ◽  
Experimental Colitis ◽  
Therapeutic Benefit ◽  
The Body ◽  
Myeloperoxidase Activity ◽  
Matrix Remodeling ◽  
Inflammatory Models ◽  
Anti Inflammatory

Methylthioadenosine (MTA) is a precursor of the methionine salvage pathway and has been shown to have anti-inflammatory properties in various models of acute and chronic inflammation. However, the anti-inflammatory properties of MTA in models of intestinal inflammation are not defined. We hypothesized that orally administered MTA would be bioavailable and reduce morbidity associated with experimental colitis. We examined clinical, histological, and molecular markers of disease in mice provided oral MTA before (preventative) or after (therapy) the induction of colitis with 3% dextran sulfate sodium (DSS). We found a reduction in disease activity, weight loss, myeloperoxidase activity, and histological damage in mice given preventative MTA compared with DSS alone. We also found that equivalent supplementation with methionine could not reproduce the anti-inflammatory effects of MTA, and that MTA had no detectable adverse effects in control or DSS mice. Expression microarray analysis of colonic tissue showed several dominant pathways related to inflammatory cytokines/chemokines and extracellular matrix remodeling were upregulation by DSS and suppressed in MTA-supplemented mice. MTA is rapidly absorbed in the gastrointestinal tract and disseminated throughout the body, based on a time course analysis of an oral bolus of MTA. This effect is transient, with MTA levels falling to near baseline within 90 min in most organs. Moreover, MTA did not lead to increased blood or tissue methionine levels, suggesting that its effects are specific. However, MTA provided limited therapeutic benefit when administered after the onset of colitis. Our results show that oral MTA supplementation is a safe and effective strategy to prevent inflammation and tissue injury associated with DSS colitis in mice. Additional studies in chronic inflammatory models are necessary to determine if MTA is a safe and beneficial option for the maintenance of remission in human inflammatory bowel disease.

scholarly journals Aqueous extract from Ipomoea asarifolia (Convolvulaceae) leaves and its phenolic compounds have anti-inflammatory activity in murine models of edema, peritonitis and air-pouch inflammation

2016 ◽  
Vol 192 ◽  
pp. 225-235 ◽  
Author(s):  
Allanny A. Furtado ◽  
Manoela Torres-Rêgo ◽  
Maíra C.J.S. Lima ◽  
Mariana A.O. Bitencourt ◽  
Andréia Bergamo Estrela ◽  
...  
Keyword(s):  
Phenolic Compounds ◽  
Aqueous Extract ◽  
Inflammatory Activity ◽  
Murine Models ◽  
Air Pouch ◽  
Anti Inflammatory ◽  
Ipomoea Asarifolia

scholarly journals Protective Effect ofCalculus Bovis Sativuson Dextran Sulphate Sodium-Induced Ulcerative Colitis in Mice

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Xiping Li ◽  
Yanjiao Xu ◽  
Chengliang Zhang ◽  
Li Deng ◽  
Mujun Chang ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Protective Effect ◽  
Activity Index ◽  
Disease Activity Index ◽  
Inflammatory Cells ◽  
Dextran Sulphate ◽  
Colon Tissue ◽  
Sod Activity ◽  
Dextran Sulphate Sodium ◽  
Anti Inflammatory

Calculus Bovis Sativus(CBS) is a commonly used traditional Chinese medicine, which has been reported to exhibit antispasmodic, fever-reducing, anti-inflammatory, and gallbladder-repairing effects. The present study aims to investigate the protective effect of CBS on dextran sulphate sodium- (DSS-) induced ulcerative colitis (UC) in mice. C57BL/6 male mice were exposed to 5% DSS in drinking water. CBS was given orally at 50 and 150 mg/kg once per day for 7 days. Body weight, disease activity index (DAI), colon length, colonic myeloperoxidase (MPO) activity, superoxide dismutase (SOD) activity, and malondialdehyde (MDA) and nitric oxide (NO) levels were measured. Administration of CBS significantly reserved these changes, decreased the MPO activity and MDA and NO level, and increased the SOD activity in the colon tissue. Histological observation suggested that CBS alleviated edema, mucosal damage, and inflammatory cells infiltration induced by DSS in the colon. Moreover, CBS significantly downregulated the mRNA expression of tumor necrosis factor-α(TNF-α), interleukin- (IL-) 1βand IL-6 in the colon tissue. Our data suggested that CBS exerted protective effect on DSS-induced UC partially through the antioxidant and anti-inflammatory activities.

scholarly journals Alleviative Effects of Exopolysaccharide Produced by Lactobacillus helveticus KLDS1.8701 on Dextran Sulfate Sodium-Induced Colitis in Mice

2021 ◽  
Vol 9 (10) ◽  
pp. 2086
Author(s):  
Yin Liu ◽  
Shujuan Zheng ◽  
Jiale Cui ◽  
Tingting Guo ◽  
Jingtao Zhang ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Inflammatory Cytokines ◽  
Intestinal Inflammation ◽  
Activity Index ◽  
Lactobacillus Helveticus ◽  
Mucosal Barrier ◽  
Microbiota Composition ◽  
Mucosal Barrier Function ◽  
Anti Inflammatory ◽  
Gut Microbiota Composition

Ulcerative colitis (UC) is a non-specific chronic inflammatory disease with lesions located in the colon and rectum. The aim of this study was to evaluate the anti-inflammatory effects of exopolysaccharide-1 (EPS-1) isolated by L. helveticus KLDS1.8701 on UC. The anti-inflammatory effects of EPS-1 were studied using dextran sulphate sodium (DSS)-induced UC model. In vivo results showed that EPS-1 administration significantly ameliorated weight loss, colon shortening, disease activity index (DAI) score, myeloperoxidase (MPO) activity, and colon tissue damage. In addition, EPS-1 administration significantly decreased the levels of pro-inflammatory cytokines and increased levels of anti-inflammatory cytokines. Meanwhile, EPS-1 administration significantly up-regulated the expression of tight junction proteins and mucin. Furthermore, EPS-1 administration modulated gut microbiota composition caused by DSS and increased the short-chain fatty acids (SCFAs) levels. Collectively, our study showed the alleviative effects of EPS- isolated by L. helveticus KLDS1.8701 on DSS-induced UC via alleviating intestinal inflammation, improving mucosal barrier function, and modulating gut microbiota composition.

scholarly journals Activation of Free Fatty Acid Receptor 4 Affects Intestinal Inflammation and Improves Colon Permeability in Mice

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2716
Author(s):  
Maciej Salaga ◽  
Adrian Bartoszek ◽  
Agata Binienda ◽  
Julia B. Krajewska ◽  
Adam Fabisiak ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Intestinal Inflammation ◽  
Feeding Habits ◽  
Inflammatory Activity ◽  
Intestinal Barrier Function ◽  
Pharmacological Intervention ◽  
Myeloperoxidase Activity ◽  
Trinitrobenzenesulfonic Acid ◽  
Anti Inflammatory

Diet is considered an important trigger in inflammatory bowel diseases (IBD), as feeding habits can affect intestinal permeability and clearance of bacterial antigens, consequently influencing the immune system. Free fatty acid receptors (FFARs), expressed on the intestinal epithelial cells, belong to the family of luminal-facing receptors that are responsive to nutrients. The objective of this study was to characterize the anti-inflammatory activity and the effect on intestinal barrier function of synthetic FFAR agonists in mouse models of colitis. Therapeutic activity of GW9508 (FFAR1 agonist), 4-CMTB (FFAR2 agonist), AR420626 (FFAR3 agonist), and GSK137647 (FFAR4 agonist) was investigated in two models of semi-chronic colitis: induced by trinitrobenzenesulfonic acid (TNBS), mimicking Crohn’s disease, as well as induced by dextran sulfate sodium (DSS), which recapitulates ulcerative colitis in humans. Moreover, we assessed the influence of FFARs agonists on epithelial ion transport and measured the ion flow stimulated by forskolin and veratridine. Administration of FFAR4 agonist GSK137647 attenuated both TNBS-induced and DSS-induced colitis in mice, as indicated by macroscopic parameters and myeloperoxidase activity. The action of FFAR4 agonist GSK137647 was significantly blocked by pretreatment with selective FFAR4 antagonist AH7614. Moreover, FFAR1 and FFAR4 agonists reversed the increase in the colon permeability caused by inflammation. FFAR4 restored the tight junction genes expression in mouse colon. This is the first evaluation of the anti-inflammatory activity of selective FFAR agonists, showing that pharmacological intervention targeting FFAR4, which is a sensor of medium and long chain fatty acids, attenuates intestinal inflammation.

scholarly journals Idebenone Protects against Spontaneous Chronic Murine Colitis by Alleviating Endoplasmic Reticulum Stress and Inflammatory Response

Biomedicines ◽  
2020 ◽  
Vol 8 (10) ◽  
pp. 384 ◽  
Author(s):  
Sonia Shastri ◽  
Tanvi Shinde ◽  
Agampodi Promoda Perera ◽  
Nuri Gueven ◽  
Rajaraman Eri
Keyword(s):  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Intestinal Inflammation ◽  
Activity Index ◽  
Goblet Cells ◽  
Inflammatory Activity ◽  
Mrna Levels ◽  
Anti Inflammatory ◽  
The Impact ◽  
Chronic Intestinal Inflammation

Endoplasmic reticulum (ER) stress in intestinal secretory goblet cells has been linked to the development of ulcerative colitis (UC). Emerging evidence suggests that the short chain quinone drug idebenone displays anti-inflammatory activity in addition to its potent antioxidant and mitochondrial electron donor properties. This study evaluated the impact of idebenone in Winnie mice, that are characterized by spontaneous chronic intestinal inflammation and ER stress caused by a missense mutation in the mucin MUC2 gene. Idebenone (200 mg/kg) was orally administered daily to 5–6 weeks old Winnie mice over a period of 21 days. Idebenone treatment substantially improved body weight gain, disease activity index (DAI), colon length and histopathology score. Immunohistochemistry revealed increased expression of MUC2 protein in goblet cells, consistent with increased MUC2 mRNA levels. Furthermore, idebenone significantly reduced the expression of the ER stress markers C/EBP homologous protein (CHOP), activating transcription factor 6 (ATF6) and X-box binding protein-1 (XBP-1) at both mRNA and protein levels. Idebenone also effectively reduced pro-inflammatory cytokine levels in colonic explants. Taken together, these results indicate that idebenone could represent a potential therapeutic approach against human UC by its strong anti-inflammatory activity and its ability to reduce markers of ER stress.

scholarly journals Intestinal inflammation increases convulsant activity and reduces antiepileptic drug efficacy in a mouse model of epilepsy

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Carmen De Caro ◽  
Antonio Leo ◽  
Valentina Nesci ◽  
Carla Ghelardini ◽  
Lorenzo di Cesare Mannelli ◽  
...  
Keyword(s):  
Antiepileptic Drug ◽  
Intestinal Inflammation ◽  
Activity Index ◽  
Disease Activity Index ◽  
Drug Efficacy ◽  
Seizure Threshold ◽  
Seizure Susceptibility ◽  
Gut Health ◽  
Anti Inflammatory ◽  
Animal Models Of Epilepsy

Abstract We studied the effects of intestinal inflammation on pentylenetetrazole (PTZ)-induced seizures in mice and the effects thereon of some antiepileptic and anti-inflammatory treatments to establish if a link may exist. The agents tested were: alpha-lactoalbumin (ALAC), a whey protein rich in tryptophan, effective in some animal models of epilepsy and on colon/intestine inflammation, valproic acid (VPA), an effective antiepileptic drug in this seizure model, mesalazine (MSZ) an effective aminosalicylate anti-inflammatory treatment against ulcerative colitis and sodium butyrate (NaB), a short chain fatty acid (SCFA) normally produced in the intestine by gut microbiota, important in maintaining gut health and reducing gut inflammation and oxidative stress. Intestinal inflammation was induced by dextran sulfate sodium (DSS) administration for 6 days. Drug treatment was started on day 3 and lasted 11 days, when seizure susceptibility to PTZ was measured along with intestinal inflammatory markers (i.e. NF-κB, Iκ-Bα, COX-2, iNOS), histological damage, disease activity index (DAI) and SCFA concentration in stools. DSS-induced colitis increased seizure susceptibility and while all treatments were able to reduce intestinal inflammation, only ALAC and NaB exhibited significant antiepileptic properties in mice with induced colitis, while they were ineffective as antiepileptics at the same doses in control mice without colitis. Interestingly, in DSS-treated mice, VPA lost part of its antiepileptic efficacy in comparison to preventing seizures in non-DSS-treated mice while MSZ remained ineffective in both groups. Our study demonstrates that reducing intestinal inflammation through ALAC or NaB administration has specific anticonvulsant effects in PTZ-treated mice. Furthermore, it appears that intestinal inflammation may reduce the antiepileptic effects of VPA, although we confirm that it decreases seizure threshold in this group. Therefore, we suggest that intestinal inflammation may represent a valid antiepileptic target which should also be considered as a participating factor to seizure incidence in susceptible patients and also could be relevant in reducing standard antiepileptic drug efficacy.

P154 THE ANTI-INFLAMMATORY EFFECT OF A PLANT-BASED DIET IN DSS-INDUCED COLITIS

2020 ◽  
Vol 26 (Supplement_1) ◽  
pp. S7-S7
Author(s):  
Abigail Basson ◽  
Danielle Kulpins ◽  
Alexandria LaSalla ◽  
Luca Di Martino ◽  
Alexander Rodriguez-Palacios ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Protective Effect ◽  
16S Rrna Gene Sequencing ◽  
Rrna Gene ◽  
Myeloperoxidase Activity ◽  
Dietary Interventions ◽  
Real Time Quantitative Pcr ◽  
Before And After ◽  
Anti Inflammatory ◽  
Inflammatory Effect

Abstract Background Inflammatory Bowel Disease (IBD) results from an imbalanced immune response toward the gut microbiota. Disruptions in the gut microbiota are proposed as critical elements that could foster pro-inflammatory imbalances and cause active flares IBD. Diet has been shown to have a pro-inflammatory effect in Crohn’s disease (CD) but not much is known on the anti-inflammatory effect of a plant-based diet. Gut microbial modulation via diet is a needed strategy for the therapeutic management of CD; however, no specific recommendations exist for CD patients. We hypothesized that plant-based diet may have a protective effect on the severity of acute dextran sodium sulfate (DSS)-induced colitis. Methods 20-wk old age-sex matched C57BL/6 mice were fed a plant-based diet or standard chow for 7 days. Mice were then administered 3% DSS for 7 days and sacrificed 2 days later. Mice were individually caged and maintained on Aspen bedding. A fecal homogenization protocol was performed prior to the start of the experiment. We monitored body weight, fecal myeloperoxidase activity, water and food intake in all mice. Epithelial permeability (FITC-dextran) and endoscopic assessment were performed before and after DSS treatment. Post mortem blood, mesenteric lymph node, colon and liver were collected. Colon morphology was evaluated using 3D-stereomicroscopy. Histological assessment was performed in a blinded manner. Analysis of samples by Illumina 16S protocols, real-time quantitative PCR (qPCR), flow cytometry. Results Mice fed the plant-based diet had decreased DSS-induced weight loss, myeloperoxidase activity and mortality compared to chow-fed mice (P<0.05). Plant-fed mice also had significantly lower colonoscopy and histological scores, with colonoscopic images showing decreased transparency and increased presence of erosion and strictures in chow-fed mice. Compared to the chow-fed mice, the concentration of FITC-D in the plasma of plant-fed mice was significantly lower (Mann-Whitney P=0.004, power 0.98). Bacterial quantification qPCR CT-values (DNA copy abundance) revealed differences in the microbiota composition with increased abundance for Lactobacilli in the context of a generic/universal 16S bacterial primer and the host gut cell DNA copies using β-actin in the plant diet mice. Illumina 16S rRNA gene sequencing of fecal genomic DNA samples is in progress. Conclusion Our results show that a plant-based diet has a protective effect on DSS-induced colitis. Further studies are needed to investigate the potential underlying mechanisms. These findings may have great potential for therapeutic dietary interventions in individuals with IBD.

Cyclooxygenase-2-derived prostaglandin D2 is an early anti-inflammatory signal in experimental colitis

2000 ◽  
Vol 279 (1) ◽  
pp. G238-G244 ◽  
Author(s):  
Maureen N. Ajuebor ◽  
Anita Singh ◽  
John L. Wallace
Keyword(s):  
Activity Index ◽  
Experimental Colitis ◽  
Cyclooxygenase 2 ◽  
Trinitrobenzene Sulfonic Acid ◽  
Prostaglandin D2 ◽  
Myeloperoxidase Activity ◽  
Granulocyte Infiltration ◽  
Inflammatory Bowel ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

The ability of nonsteroidal anti-inflammatory drugs and cyclooxygenase-2 inhibitors to exacerbate inflammatory bowel disease suggests that prostaglandins are important anti-inflammatory mediators in this context. Prostaglandin D2 has been suggested to exert anti-inflammatory effects. We investigated the possibility that prostaglandin D2 derived from cyclooxygenase-2 plays an important role in downregulating colonic inflammation in rats. Colitis was induced by intracolonic administration of trinitrobenzene sulfonic acid. At various times thereafter (from 1 h to 7 days), colonic prostaglandin synthesis and myeloperoxidase activity (index of granulocyte infiltration) were measured. Prostaglandin D2synthesis was elevated >4-fold above controls within 1–3 h of induction of colitis, preceding significant granulocyte infiltration. Treatment with a selective cyclooxygenase-2 inhibitor abolished the increase in prostaglandin D2 synthesis and caused a doubling of granulocyte infiltration. Colonic granulocyte infiltration was significantly reduced by administration of prostaglandin D2 or a DP receptor agonist (BW-245C). These results demonstrate that induction of colitis results in a rapid increase in prostaglandin D2 synthesis via cyclooxygenase-2. Prostaglandin D2 downregulates granulocyte infiltration into the colonic mucosa, probably through the DP receptor.

Protective effect of telmisartan treatment against arsenic-induced testicular toxicity in rats

2015 ◽  
Vol 70 (7-8) ◽  
pp. 175-181 ◽  
Author(s):  
Amr A. Fouad ◽  
Waleed H. Albuali ◽  
Abdulruhman S. Al-Mulhim ◽  
Iyad Jresat
Keyword(s):  
Nitric Oxide ◽  
Protective Effect ◽  
Sodium Arsenite ◽  
Nitrosative Stress ◽  
Testicular Tissue ◽  
Myeloperoxidase Activity ◽  
Potential Candidate ◽  
Testicular Damage ◽  
Angiotensin Ii Receptor ◽  
Anti Inflammatory

Abstract Oxidative/nitrosative stress, inflammation, and apoptosis play a crucial role in the pathogenesis of arsenic-induced testicular injury. Telmisartan, the angiotensin II-receptor antagonist, possesses antioxidant and anti-inflammatory activities. The protective effect of telmisartan against arsenic-induced testicular damage was investigated in rats. Testicular damage was induced by sodium arsenite (10 mg kg–1/day, p.o., for 2 consecutive days). Telmisartan (10 mg kg–1/day, i.p.) was given for 3 consecutive days, starting 1 day before sodium arsenite administration. Telmisartan significantly attenuated the arsenic-induced decrease in the levels of serum testosterone and testicular reduced glutathione, and significantly decreased the elevation of the levels of testicular malondialdehyde, nitric oxide, and arsenic levels, as well as myeloperoxidase activity resulting from sodium arsenite administration. Histopathological and immunohistochemical examination revealed that telmisartan markedly attenuated testicular tissue changes, and decreased the arsenic-induced expression of vascular endothelial growth factor, inducible nitric oxide synthase, tumor necrosis factor-α, cyclooxygenase-2, nuclear factor-κB, and caspase-3. Telmisartan, via its antioxidant and/or anti-inflammatory effects, may represent a potential candidate to protect against the deleterious effects of arsenic on testicular tissue.

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