scholarly journals Preparation of Herbal Formulation for Inflammatory Bowel Disease Based on In Vitro Screening and In Vivo Evaluation in a Mouse Model of Experimental Colitis

Molecules ◽  
2019 ◽  
Vol 24 (3) ◽  
pp. 464 ◽  
Author(s):  
Jaemin Lee ◽  
Han-Seok Choi ◽  
Jinkyung Lee ◽  
Jimin Park ◽  
Sang-Back Kim ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Inflammatory Activity ◽  
In Vitro Screening ◽  
Screening Experiments ◽  
Tnf Α ◽  
Inflammatory Bowel ◽  
Anti Inflammatory ◽  
Colitis Model

Many medicinal plants have been used traditionally in East Asia for the treatment of gastrointestinal disease and inflammation. The aim of this study was to evaluate the anti-inflammatory activity of 350 extracts (175 water extracts and 175 ethanol extracts) from 71 single plants, 97 mixtures of two plants, and seven formulations based on traditional medicine, to find herbal formulations to treat inflammatory bowel disease (IBD). In the in vitro screening, nitric oxide (NO), tumor necrosis factor (TNF)-α, and interleukin (IL)-6 levels were determined in LPS-treated RAW264.7 cells and the TNF-α induced monocyte-epithelial cell adhesion assay was used for the evaluation of the anti-inflammatory activity of the compounds. Dextran sulfate sodium (DSS)-induced colitis model and 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model were used to evaluate the therapeutic effect against IBD of the samples selected from the in vitro screening. KM1608, composed of Zingiber officinale, Terminalia chebula and Aucklandia lappa, was prepared based on the screening experiments. The oral administration of KM1608 significantly attenuated the severity of colitis symptoms, such as weight loss, diarrhea, and rectal bleeding, in TNBS-induced colitis. In addition, inflammatory mediators, such as myeloperoxidase, TNF-α, and IL-6 levels decreased in the lysate of colon tissues treated with KM1608. Collectively, KM1608 ameliorated colitis through the regulation of inflammatory responses within the colon, which indicated that KM1608 had potential for the treatment of IBD.

scholarly journals Food and Food Groups in Inflammatory Bowel Disease (IBD): The Design of the Groningen Anti-Inflammatory Diet (GrAID)

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1067
Author(s):  
Marjo J. E. Campmans-Kuijpers ◽  
Gerard Dijkstra
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Food Group ◽  
Dietary Guidelines ◽  
Current Evidence ◽  
Group Level ◽  
Food Groups ◽  
Inflammatory Bowel ◽  
Anti Inflammatory

Diet plays a pivotal role in the onset and course of inflammatory bowel disease (IBD). Patients are keen to know what to eat to reduce symptoms and flares, but dietary guidelines are lacking. To advice patients, an overview of the current evidence on food (group) level is needed. This narrative review studies the effects of food (groups) on the onset and course of IBD and if not available the effects in healthy subjects or animal and in vitro IBD models. Based on this evidence the Groningen anti-inflammatory diet (GrAID) was designed and compared on food (group) level to other existing IBD diets. Although on several foods conflicting results were found, this review provides patients a good overview. Based on this evidence, the GrAID consists of lean meat, eggs, fish, plain dairy (such as milk, yoghurt, kefir and hard cheeses), fruit, vegetables, legumes, wheat, coffee, tea and honey. Red meat, other dairy products and sugar should be limited. Canned and processed foods, alcohol and sweetened beverages should be avoided. This comprehensive review focuses on anti-inflammatory properties of foods providing IBD patients with the best evidence on which foods they should eat or avoid to reduce flares. This was used to design the GrAID.

A moderately elevated soy protein diet mitigates inflammatory changes in gut and in bone turnover during chronic TNBS-induced inflammatory bowel disease

2019 ◽  
Vol 44 (6) ◽  
pp. 595-605 ◽  
Author(s):  
Corinne E. Metzger ◽  
S. Anand Narayanan ◽  
David C. Zawieja ◽  
Susan A. Bloomfield
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bone Turnover ◽  
Soy Protein ◽  
Bowel Disease ◽  
Protein Diet ◽  
Trinitrobenzene Sulfonic Acid ◽  
Inflammatory Bowel ◽  
Anti Inflammatory ◽  
The Impact ◽  
Colitis Model

Inflammatory bowel disease is a condition that leads to gut pathologies such as abnormal lymphatic architecture, as well as to systemic comorbidities such as bone loss. Furthermore, current therapies are limited to low efficacy and incur side effects. Dietary interventions have been explored minimally, but may provide a treatment for improving gut outcomes and comorbidities. Indeed, plant-based soy protein has been shown to exert anti-inflammatory effects. Here, we tested the impact of a moderately elevated soy protein diet in a chronic, 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model on gut and bone inflammatory-mediated pathophysiological adaptations. Colitis was induced by intrarectal administration of TNBS. Gut histopathology was scored, and lymphatic structural changes and the local inflammatory state were assessed via immunofluorescence. In addition, the effects of gut inflammation on bone turnover and osteocyte proteins were determined via histomorphometry and immunohistochemistry, respectively. The moderately elevated soy protein diet produced improvements in both colonic and bone tissues. In TNBS animals given the soy protein intervention, colon histological scores were reduced and the abnormal lymphatic architecture resolved. There were also improvements in bone formation and reduced bone resorption. In addition, TNBS increased inflammatory cytokines such as tumor necrosis factor-α and receptor activator of nuclear factor κ-B ligand in the gut and bone, but this was resolved in both tissues with the dietary soy protein intervention. The moderately elevated soy protein diet mitigated gut and bone inflammation in a chronic, TNBS-induced colitis model, demonstrating the potential for soy protein as a potential anti-inflammatory dietary intervention for inflammatory bowel disease.

scholarly journals Synthesis and evaluation of 6-heteroarylamino-2,4,5-trimethylpyridin-3-ols as inhibitors of TNF-α-induced cell adhesion and inflammatory bowel disease

MedChemComm ◽  
2018 ◽  
Vol 9 (8) ◽  
pp. 1305-1310 ◽  
Author(s):  
Sang Won Park ◽  
Suhrid Banskota ◽  
Pallavi Gurung ◽  
You Jin Jin ◽  
Han-eol Kang ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Cell Adhesion ◽  
Bowel Disease ◽  
Tnf Α ◽  
Inflammatory Bowel ◽  
Anti Inflammatory

Novel series of anti-inflammatory bowel disease (IBD) agent was identified through TNF-α-induced cell adhesion.

scholarly journals DOP53 PTPN2 and TiO2 in the pathogenesis of inflammatory bowel disease

2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S092-S092
Author(s):  
J Conde ◽  
M Schwarzfischer ◽  
E Katkeviciute ◽  
J Häfliger ◽  
A Niechcial ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Flow Cytometry ◽  
Titanium Dioxide ◽  
Bowel Disease ◽  
Myeloid Cells ◽  
Food Additive ◽  
Inflammasome Activation ◽  
Inflammatory Bowel ◽  
Anti Inflammatory

Abstract Background Inflammatory bowel disease (IBD) is caused by a complex interaction among genetic, immunological, bacterial and environmental factors. In this scenario, protein tyrosine phosphatase non-receptor type-2 (PTPN2) has been recognised as a risk factor for the development of IBD and functional studies revealed a major role for this protein in the development of experimental colitis through the regulation of the inflammasome, among other processes. In the same way, a potential relationship between diet components and IBD was suggested. In fact, it was reported that the food additive titanium dioxide (TiO2) was able to induce inflammasome activation in vitro and increase colitis severity in vivo. These observations led us to hypothesise a putative relationship between PTPN2 and TiO2 that could explain the effects of this microparticle in the pathogenesis of bowel inflammation. Methods DSS colitis model was performed in mice lacking PTPN2 in myeloid cells and their wild-type littermates, treated or not with titanium dioxide. After that, histology studies, flow cytometry, expression analysis, ELISA and barrier function experiments were performed. Also, bone marrow-derived macrophages (BMDMs) were used for in vitro studies. Results Titanium dioxide was able to exacerbate DSS-induced colitis, especially in mice lacking PTPN2 in myeloid cells. Flow cytometry analysis of the lamina propria revealed significant changes in different immune cell populations such as macrophages. In vitro experiments using BMDMs revealed that TiO2 induced the activation of the inflammasome. Also, this microparticle down-regulated the expression of the anti-inflammatory cytokine IL-10 and these effects were mainly mediated by JNK and ERK kinases. Conclusions The food additive titanium dioxide seems to play a negative role in colitis development by affecting the production of pro- and anti-inflammatory mediators in macrophages. This study reveals a new mechanism by which a certain component of the diet modulates intestinal inflammation.

scholarly journals Immunomodulatory role of Parkinson’s disease 7 in inflammatory bowel disease

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Rita Lippai ◽  
Apor Veres-Székely ◽  
Erna Sziksz ◽  
Yoichiro Iwakura ◽  
Domonkos Pap ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Inflammatory Bowel Disease ◽  
Parkinson's Disease ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Tnf Α ◽  
Inflammatory Bowel ◽  
Ht 29

AbstractRecently the role of Parkinson’s disease 7 (PARK7) was studied in gastrointestinal diseases, however, the complex role of PARK7 in the intestinal inflammation is still not completely clear. Expression and localization of PARK7 were determined in the colon biopsies of children with inflammatory bowel disease (IBD), in the colon of dextran sodium sulphate (DSS) treated mice and in HT-29 colonic epithelial cells treated with interleukin (IL)-17, hydrogen peroxide (H2O2), tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β or lipopolysaccharide (LPS). Effect of PARK7 on the synthesis of IBD related cytokines was determined using PARK7 gene silenced HT-29 cells and 3,4,5-trimethoxy-N-(4-(8-methylimidazo(1,2-a)pyridine-2-yl)phenyl)benzamide (Comp23)—compound increasing PARK7 activity—treated mice with DSS-colitis. PARK7 expression was higher in the mucosa of children with Crohn’s disease compared to that of controls. While H2O2 and IL-17 treatment increased, LPS, TNF-α or TGF-β treatment decreased the PARK7 synthesis of HT-29 cells. PARK7 gene silencing influenced the synthesis of IL1B, IL6, TNFA and TGFB1 in vitro. Comp23 treatment attenuated the ex vivo permeability of colonic sacs, the clinical symptoms, and mucosal expression of Tgfb1, Il1b, Il6 and Il10 of DSS-treated mice. Our study revealed the role of PARK7 in the regulation of IBD-related inflammation in vitro and in vivo, suggesting its importance as a future therapeutic target.

Levels of NAD+-dependent 15-hydroxyprostaglandin dehydrogenase are reduced in inflammatory bowel disease: evidence for involvement of TNF-α

2006 ◽  
Vol 290 (2) ◽  
pp. G361-G368 ◽  
Author(s):  
Taisuke Otani ◽  
Kentaro Yamaguchi ◽  
Ellen Scherl ◽  
Baoheng Du ◽  
Hsin-Hsiung Tai ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Colonic Mucosa ◽  
Prostaglandin E ◽  
Tnf Α ◽  
Normal Colonic Epithelium ◽  
Inflammatory Bowel ◽  
In Vitro Treatment

Increased amounts of PGE2 have been detected in the inflamed mucosa of patients with inflammatory bowel disease (IBD). This increase has been attributed to enhanced synthesis rather than reduced catabolism of PGE2. 15-Hydroxyprostaglandin dehydrogenase (15-PGDH) plays a major role in the catabolism of PGE2. In this study, we investigated whether amounts of 15-PGDH were altered in inflamed mucosa from patients with IBD. Amounts of 15-PGDH protein and mRNA were markedly reduced in inflamed mucosa from patients with Crohn's disease and ulcerative colitis. In situ hybridization demonstrated that 15-PGDH was expressed in normal colonic epithelium but was virtually absent in inflamed colonic mucosa from IBD patients. Because of the importance of TNF-α in IBD, we also determined the effects of TNF-α on the expression of 15-PGDH in vitro. Treatment with TNF-α suppressed the transcription of 15-PGDH in human colonocytes, resulting in reduced amounts of 15-PGDH mRNA and protein and enzyme activity. In contrast, TNF-α induced two enzymes (cyclooxygenase-2 and microsomal prostaglandin E synthase-1) that contribute to increased synthesis of PGE2. Overexpressing 15-PGDH blocked the increase in PGE2 production mediated by TNF-α. Taken together, these results suggest that reduced expression of 15-PGDH contributes to the elevated levels of PGE2 found in inflamed mucosa of IBD patients. The decrease in amounts of 15-PGDH in inflamed mucosa can be explained at least, in part, by TNF-α-mediated suppression of 15-PGDH transcription.

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