scholarly journals Danggui Buxue Decoction Ameliorates Inflammatory Bowel Disease by Improving Inflammation and Rebuilding Intestinal Mucosal Barrier

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Chengyin Li ◽  
Fenglin Zhu ◽  
Shasha Wang ◽  
Jing Wang ◽  
Bin Wu

Objective. This study aimed to determine whether Danggui Buxue decoction (DGBX) can improve inflammatory bowel disease (IBD) by regulating immunity and promoting intestinal mucosal repair. Method. Dextran sulfate sodium (DSS) was used to induce the IBD model. Drugs (DGBX or saline) were administered to mice, which were randomly divided into three groups (control, model, and experimental groups). Hematoxylin and eosin staining of intestinal tissues was conducted to observe for morphological changes. Changes in cytokines and immune cells in the intestinal tissues were detected by enzyme-linked immunosorbent assay and flow cytometry. Immunofluorescence techniques were used to assess the status of the intestinal mucosal repair. Results. This study found that treatment with DGBX can effectively improve the inflammatory state and pathological structure of the IBD model. DGBX not only can significantly change the composition of intestinal mucosal immune cells and promote the regression of inflammation but also significantly increase the proliferation of intestinal epithelial cells and promote the rapid repair of intestinal mucosal barrier injury compared with the model group ( p < 0.05 ). Conclusion. Taking these results, DGBX shows promising protective effects on IBD by regulating immunity and promoting intestinal mucosal repair.

2018 ◽  
Vol 5 (3) ◽  
pp. 180107 ◽  
Author(s):  
Sophie C. Payne ◽  
Robert K. Shepherd ◽  
Alicia Sedo ◽  
James B. Fallon ◽  
John B. Furness

Inflammatory damage to the bowel, as occurs in inflammatory bowel disease (IBD), is debilitating to patients. In both patients and animal experimental models, histological analyses of biopsies and endoscopic examinations are used to evaluate the disease state. However, such measurements often have delays and are invasive, while endoscopy is not quantitatively objective. Therefore, a real-time quantitative method to assess compromised mucosal barrier function is advantageous. We investigated the correlation of in vivo changes in electrical transmural impedance with histological measures of inflammation. Four platinum (Pt) ball electrodes were placed in the lumen of the rat small intestine, with a return electrode under the skin. Electrodes placed within the non-inflamed intestine generated stable impedances during the 3 h testing period. Following an intraluminal injection of 2,4,6-trinitrobenzene sulfonic acid (TNBS), an established animal model of IBD, impedances in the inflamed region significantly decreased relative to a region not exposed to TNBS ( p  < 0.05). Changes in intestinal transmural impedance were correlated ( p  < 0.05) with histologically assessed damage to the mucosa and increases in neutrophil, eosinophil and T-cell populations at 3 h compared with tissue from control regions. This quantitative, real-time assay may have application in the diagnosis and clinical management of IBD.


2019 ◽  
Vol 1 (3) ◽  
Author(s):  
Jeffrey A Berinstein ◽  
Calen A Steiner ◽  
Athos Bousvaros ◽  
Felix P Tiongco ◽  
Eugene Greenberg ◽  
...  

Abstract Background Fecal calprotectin (fCAL) is a noninvasive biomarker used to differentiate between inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS). Methods A multicenter prospective case–control study evaluating the BÜHLMANN fCAL enzyme-linked immunosorbent assay (ELISA) was conducted in 478 subjects. Sensitivity, specificity, predictive values, and area under the receiver operator characteristic (AuROC) curve are reported and compared to another device. Results In differentiating IBD from IBS, the BÜHLMANN fCAL ELISA is very sensitive (93.3%) at a cutoff &lt;80 μg/g and balanced sensitivity (84.4%) and specificity (85.4%) at a cutoff &gt;160 μg/g (AuROC 0.933). Conclusions The BÜHLMANN fCAL ELISA demonstrates excellent discriminating between IBD and IBS.


2019 ◽  
Vol 2019 ◽  
pp. 1-13
Author(s):  
Weigang Shu ◽  
Zhi Pang ◽  
Chunjin Xu ◽  
Jian Lin ◽  
Gengfeng Li ◽  
...  

Anemia is one of the most common complications in patients with inflammatory bowel disease (IBD). Hepcidin as a key regulator of iron metabolism is pivotal in mediating the occurrence of anemia of chronic disease. Herein, we analyzed the levels of hepcidin in sera from IBD patients by enzyme-linked immunosorbent assay and investigated its potential role in regulating the anemia in IBD. We observed that the levels of serum hepcidin were increased in active IBD patients compared with those in remitted IBD patients and healthy controls and that serum hepcidin was associated with disease activity, CRP, and ESR, respectively. Importantly, we found that the increased levels of serum hepcidin were positively correlated with the severity of anemia and the imbalance of iron metabolism in anemic UC and CD patients. Proinflammatory factors (e.g., IL-6, IL-17, and TNF-α) were positively correlated with the concentrations of serum hepcidin in IBD patients. Interestingly, hepcidin was found to be decreased in patients with Crohn’s disease after successful therapy with anti-TNF-α mAb (i.e., infliximab), indicating the underlying association between TNF-α and hepcidin expression. To investigate the specific mechanisms involved, we cultured LO2 and HepG2 cell lines in vitro under stimulation with TNF-α and observed that the levels of hepcidin mRNA were markedly upregulated in caspase-3/8- and NF-κB-dependent manners. Therefore, our data suggest that TNF-α stimulates the expression of hepcidin in IBD patients, resulting in aggravated anemia and that blockage of TNF-α or the caspase-3/8 and NF-κB pathways could downregulate hepcidin expression. This study provides inspiration for the therapy and management of anemia in IBD.


Gut ◽  
1998 ◽  
Vol 42 (2) ◽  
pp. 214-219 ◽  
Author(s):  
M E McAlindon ◽  
C J Hawkey ◽  
Y R Mahida

Background—In the lipopolysaccharide (LPS) stimulated peripheral blood monocyte, the precursor form of interleukin 1β (IL-1β, 31 kD) is processed by IL-1β converting enzyme (ICE) to the mature, bioactive form (17 kD). IL-1β is a proinflammatory cytokine which is likely to have a role in the pathogenesis of inflammatory bowel disease (IBD).Aims—To investigate the expression and processing of IL-1β and ICE by tissue macrophages from normal and IBD colonic mucosa.Methods—Mucosal biopsy specimens and lamina propria cells from normal and IBD colons were studied by reverse transcription polymerase chain reaction (RT-PCR), western blot analysis, and ELISA (enzyme linked immunosorbent assay).Results—Normal colonic macrophages synthesised only the precursor form of IL-1β whereas in IBD the mature form was also produced. Similarly, cells from normal colonic mucosa synthesised ICE as the precursor (p45) only, whereas macrophages from IBD colons produced active (p20) ICE. Ac-Tyr-Val-Ala-Asp-CHO, a specific peptide aldehyde inhibitor of ICE, significantly reduced the amount of mature IL-1β released by isolated IBD macrophages (from a median of 1.2 (range 0.78–4.42) ng/ml to 0.43 (0.21–1.6) ng/ml; p<0.01).Conclusions—Exposure of normal colonic macrophages to LPS only induces the production of the precursor form of IL-1β, because the cells fail to activate ICE. In contrast, IBD colonic macrophages are able to activate ICE and hence release mature IL-1β in a manner similar to circulating monocytes. This is consistent with IBD macrophages being recently recruited from the circulating monocyte population. Targeted inhibition of ICE may represent a novel form of therapy in IBD.


2015 ◽  
Vol 2015 ◽  
pp. 1-4 ◽  
Author(s):  
Zehra Betül Paköz ◽  
Cem Çekiç ◽  
Mahmut Arabul ◽  
Elif Sarıtaş Yüksel ◽  
Serkan İpek ◽  
...  

Aim. While there are many well-defined serological markers for inflammatory bowel disease (IBD), there is limited evidence that they positively affect clinical outcomes. This study aimed to evaluate the correlation between hepcidin serum levels and disease activity in IBD.Materials and Methods. Eighty-five consecutive IBD patients were enrolled in the study. Hepcidin serum levels were assessed using an enzyme-linked immunosorbent assay (ELISA) and were compared with disease activity as well as the interleukin-6 (IL-6) and C-reactive protein (CRP) levels.Results. The mean hepcidin serum levels in Crohn’s disease (CD) patients in remission and in the active phase were3837±1436and3752±1274 pg/mL, respectivelyP=0.613. The mean hepcidin serum levels in ulcerative colitis (UC) patients in remission and in the active phase were4285±8623and3727±1176 pg/mL, respectivelyP=0.241. Correlation analysis between inflammatory markers and hepcidin serum levels indicated that there was no correlation between hepcidin levels and IL-6P=0.582or CRPP=0.783.Conclusion. As an acute-phase protein, hepcidin seems to have a lower efficacy than other parameters in the detection of activation in IBD.


2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Andrea Michielan ◽  
Renata D’Incà

The pathogenesis of inflammatory bowel disease (IBD) is multifactorial with data suggesting the role of a disturbed interaction between the gut and the intestinal microbiota. A defective mucosal barrier may result in increased intestinal permeability which promotes the exposition to luminal content and triggers an immunological response that promotes intestinal inflammation. IBD patients display several defects in the many specialized components of mucosal barrier, from the mucus layer composition to the adhesion molecules that regulate paracellular permeability. These alterations may represent a primary dysfunction in Crohn’s disease, but they may also perpetuate chronic mucosal inflammation in ulcerative colitis. In clinical practice, several studies have documented that changes in intestinal permeability can predict IBD course. Functional tests, such as the sugar absorption tests or the novel imaging technique using confocal laser endomicroscopy, allow anin vivoassessment of gut barrier integrity. Antitumor necrosis factor-α(TNF-α) therapy reduces mucosal inflammation and restores intestinal permeability in IBD patients. Butyrate, zinc, and some probiotics also ameliorate mucosal barrier dysfunction but their use is still limited and further studies are needed before considering permeability manipulation as a therapeutic target in IBD.


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