scholarly journals Ginger relieves intestinal hypersensitivity of diarrhea predominant irritable bowel syndrome by inhibiting proinflammatory reaction

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Changrong Zhang ◽  
Yongquan Huang ◽  
Peiwu Li ◽  
Xinlin Chen ◽  
Fengbin Liu ◽  
...  
Keyword(s):  
Irritable Bowel Syndrome ◽  
Hplc Analysis ◽  
Chemical Stimulation ◽  
Inflammatory Factors ◽  
Tnf Α ◽  
Defecation Frequency ◽  
Fecal Water ◽  
Intestinal Hypersensitivity ◽  
Irritable Bowel ◽  
Proinflammatory Factors

Abstract Background Ginger or ginger extracts have been used in traditional medicine relieve pain caused by diarrhea predominant irritable bowel syndrome (IBS-D), but few data exists about its effectiveness. This present study was to validate the effect of ginger on visceral pain, and to further explore the possible underlying mechanism by which ginger is used to relieve IBS-D intestinal hypersensitivity. Methods First, the IBS-D rat model was established by chemical stimulation and acute and chronic pressure stimulation. Then, different dose of ginger were administrated to IBS-D rats and evaluate the defecation frequency, fecal water content (FWC) and abdominal withdrawal reflex (AWR) scores in IBS-D rats. Further, the IBS-D rats were sacrificed to collecte the colonic tissues to evaluate the effect of ginger administration on its pathology and changes of pro-inflammatory factors, and changes of NF-κB pathway. Second, the ginger was taken to HPLC analysis and 6-gingerol was choosen to further experiment. Then, IBS-D rats were treated with different dose of 6-gingerol, and the behavioral evaluation were to evaluate the effect of 6-gingerol on IBS-D rats. Further, colonic epithelial cells (CECs) were collectted and to evaluate the effect of 6-gingerol on the expression of inflammatory factors and changes of NF-κB pathway. Results The IBS-D rat model was successfully established by chemical stimulation and acute and chronic pressure stimulation. And ginger treatment significantly reduced the defecation frequency, fecal water content and AWR scores in IBS-D rats. Histopathological analysis showed that ginger treatment can significantly reduce colonic edema and promote the recovery of inflammation in IBS-D rats, and the effect is equivalent to rifaximin. Elisa and RT-qPCR showed that ginger inhibited the expression of proinflammatory factors (TNF-α, IL-6, iNOS) in IBS-D rats. Western blot showed IkBα was up-regulated while p-p65 was inhibited under ginger treatment. HPLC analysis showed that 6-gingerol was the main component of ginger, which could improve clinical symptoms in IBS-D rats. Western blot and RT-qPCR showed that 6-gingerol inhibited the expression of proinflammatory factors (TNF-α, IL-6, iNOS) in CECs, and inhibition of IκBα degradation and phosphorylation of p65 involved in NF-κB pathway. Conclusion Ginger and ginger extract could relieve intestinal hypersensitivity of IBS-D by inhibiting proinflammatory response.

scholarly journals Mechanism of QingHuaZhiXie Prescription Regulating TLR4-IECs Pathway in the Intervention of Diarrhea Predominant Irritable Bowel Syndrome

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Hua Huang ◽  
Ping Zhao ◽  
Meijuan Xi ◽  
Fang Li ◽  
Lijiang Ji
Keyword(s):  
Irritable Bowel Syndrome ◽  
Intervention Group ◽  
Immunohistochemical Analysis ◽  
Inflammatory Factors ◽  
Control Group ◽  
Model Group ◽  
Expression Levels ◽  
Protein Levels ◽  
Intestinal Hypersensitivity ◽  
Irritable Bowel

To investigate the effect and mechanism of QingHuaZhiXie prescription on diarrhea predominant irritable bowel syndrome (D-IBS), animal models of rats were used in this study. 48 rats were randomly divided into 6 groups, containing one control group, one animal model group (D-IBS group), and four drug intervention groups (low, medium, and high dosage of QingHuaZhiXie prescription and trimebutine maleate intervention group). Abdominal withdrawal reflex (AWR) and Bristol stool form scale were recorded; the expression levels of inflammatory factors (TNF-α and IFN-γ), pathway proteins TLR4, MyD88, NF-κB, and key proteins of tight junction between intestinal epithelial cells (IECs) were detected; the microstructure of intestinal mucosal was observed by hematoxylin and eosin (H&E) staining; MPO activity was detected with immunohistochemical analysis to reflect the inflammation of tissues. Results show that QingHuaZhiXie prescription reduced diarrhea index and intestinal hypersensitivity and intestinal tissue integrity after intervention. MPO activity in QingHuaZhiXie prescription-treated rats was significantly lower relative to their model group. The expression levels of inflammatory factors and TLR4/MyD88/NF-κB pathway proteins were repressed, and the protein levels of occludin and claudin-1 increased. Meanwhile, this study also found that the remission effect of QingHuaZhiXie prescription on D-IBS increased with its dosage increase. Hence, as a therapeutic prescription for D-IBS, QingHuaZhiXie prescription could relieve D-IBS symptoms through balancing the inflammatory factors expression by inhibiting the TLR4/MyD88/NF-κB pathway and maintaining the function and structure of IECs by improving the protein levels of JAM, occludin, claudin-1, and ZO-1.

scholarly journals Tong-Xie-Yao-Fang improves intestinal permeability in diarrhoea-predominant irritable bowel syndrome rats by inhibiting the NF-κB and notch signalling pathways

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Qiuke Hou ◽  
Yongquan Huang ◽  
Zhaoyang Zhu ◽  
Liu Liao ◽  
Xinlin Chen ◽  
...  
Keyword(s):  
Irritable Bowel Syndrome ◽  
Intestinal Permeability ◽  
Rat Model ◽  
Distal Colon ◽  
Notch Signalling ◽  
Signalling Pathways ◽  
Model Group ◽  
Related Factors ◽  
Defecation Frequency ◽  
Irritable Bowel

Abstract Background Tong-Xie-Yao-Fang (TXYF) has been shown to be effective in diarrhoea-predominant irritable bowel syndrome (IBS-D) patients. However, the underlying mechanism remains to be clarified. The aim of this study was to investigate the efficacy and related mechanisms of TXYF in an IBS-D rat model. Methods The IBS-D rat model was established with 4% acetic acid and evaluated by haematoxylin-eosin (HE) staining. Then, IBS-D rats were divided into control, TXYF and rifaximin groups and treated intragastrically with normal saline, TXYF and rifaximin, respectively, for 14 days. The following indicators were measured before and after treatment: defecation frequency, faecal water content (FWC) and colorectal distension (CRD). Histopathological changes in the distal colon were observed after treatment. The expression of OCLN and ZO1 in the distal colon of IBS-D rats reflected the intestinal mucosal permeability, as measured by qRT-PCR, western blot, and enzyme-linked immunosorbent assays (ELISAs). The NF-κB and Notch signalling pathways and inflammation-related factors were investigated. Results After treatment with TXYF, the defecation frequency, FWC and CRD were significantly lower than those in the model group (P < 0.05). HE staining showed that colonic epithelial cells (CECs) in the IBS-D rats displayed significant oedema, impaired intestinal mucosal integrity and an increased influx of inflammatory cells. A significant reduction in granulocyte and CEC oedema was observed after the administration of TXYF and rifaximin compared to that of the model group and blank group (P < 0.05). TXYF significantly upregulated the expression of OCLN and ZO-1 and downregulated inflammation-related factors (IL-6, IL-1β, and TNF-α and the chemokine KC) in IBS-D rats compared to those in the model group rats (P < 0.05). In terms of the NF-κB and Notch signalling pathways, the expression of NICD, p-ERK, Hes-1 and p-P65 decreased significantly in the TXYF and rifaximin groups, while the expression of ATOH1 increased significantly compared to that in the model group (P < 0.05). Conclusion TXYF can effectively improve intestinal permeability and enhance intestinal mucosal barrier function, which may be related to inhibition of the inflammatory cascade and the NF-κB and Notch signalling pathways.

Total polysaccharides of adlay bran (Coix lachryma-jobi L.) improve TNF-α induced epithelial barrier dysfunction in Caco-2 cells via inhibition of the inflammatory response

2019 ◽  
Vol 10 (5) ◽  
pp. 2906-2913 ◽  
Author(s):  
Yanlong Li ◽  
Xudong Tian ◽  
Shengcai Li ◽  
Lijun Chang ◽  
Ping Sun ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Irritable Bowel Syndrome ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Barrier Dysfunction ◽  
Intestinal Epithelial Barrier ◽  
Tnf Α ◽  
Inflammatory Bowel ◽  
Irritable Bowel ◽  
Epithelial Barrier Dysfunction

Dysfunction of the intestinal epithelial barrier plays an important role in the pathogenesis of several intestinal diseases, including celiac disease, inflammatory bowel disease, and irritable bowel syndrome.

IFN-γ and TNF-α decrease serotonin transporter function and expression in Caco2 cells

2007 ◽  
Vol 292 (3) ◽  
pp. G779-G784 ◽  
Author(s):  
Kevin F. Foley ◽  
Cristen Pantano ◽  
Allison Ciolino ◽  
Gary M. Mawe
Keyword(s):  
Ulcerative Colitis ◽  
Irritable Bowel Syndrome ◽  
Conditioned Medium ◽  
Human Lymphocytes ◽  
Protein Levels ◽  
Tnf Α ◽  
Ifn Γ ◽  
5 Ht Uptake ◽  
Irritable Bowel

Recent studies have shown that mucosal serotonin (5-HT) transporter (SERT) expression is decreased in animal models of colitis, as well as in the colonic mucosa of humans with ulcerative colitis and irritable bowel syndrome. Altered SERT function or expression may underlie the altered motility, secretion, and sensation seen in these inflammatory gut disorders. In an effort to elucidate possible mediators of SERT downregulation, we treated cultured colonic epithelial cells (Caco2) with conditioned medium from activated human lymphocytes. Application of the conditioned medium caused a decrease in fluoxetine-sensitive [3H]5-HT uptake. Individual proinflammatory agents were then tested for their ability to affect uptake. Cells were treated for 48 or 72 h with PGE2 (10 μM), IFN-γ (500 ng/ml), TNF-α (50 ng/ml), IL-12 (50 ng/ml), or the nitric oxide-releasing agent S-nitrosoglutathione (GSNO; 100 μM). [3H]5-HT uptake was then measured. Neither PGE nor IL-12 had any effect on [3H]5-HT uptake, and GSNO increased uptake. However, after 3-day incubation, both TNF-α and IFN-γ elicited significant decreases in SERT function. Neither TNF-α nor IFN-γ were cytotoxic when used for this period of time and at these concentrations. These two cytokines also induced decreases in SERT mRNA and protein levels. By altering SERT expression, TNF-α and IFN-γ could contribute to the altered motility and expression seen in vivo in ulcerative colitis or irritable bowel syndrome.

scholarly journals Fatigue in irritable bowel syndrome is associated with plasma levels of TNF-α and mesocorticolimbic connectivity

2020 ◽  
Author(s):  
Anna-Karin Norlin ◽  
Susanna Walter ◽  
Adriane Icenhour ◽  
Åsa V. Keita ◽  
Sigrid Elsenbruch ◽  
...  
Keyword(s):  
Irritable Bowel Syndrome ◽  
Plasma Levels ◽  
Tnf Α ◽  
Irritable Bowel

scholarly journals Epstein-Barr Virus BZLF1-Mediated Downregulation of Proinflammatory Factors Is Essential for Optimal Lytic Viral Replication

2015 ◽  
Vol 90 (2) ◽  
pp. 887-903 ◽  
Author(s):  
Yuqing Li ◽  
Xubing Long ◽  
Lu Huang ◽  
Mengtian Yang ◽  
Yan Yuan ◽  
...  
Keyword(s):  
Viral Replication ◽  
Epstein Barr Virus ◽  
Lytic Cycle ◽  
Inflammatory Factors ◽  
Barr Virus ◽  
Ebv Infection ◽  
Tnf Α ◽  
Ifn Γ ◽  
Epstein Barr ◽  
Proinflammatory Factors

ABSTRACTElevated secretion of inflammatory factors is associated with latent Epstein-Barr virus (EBV) infection and the pathology of EBV-associated diseases; however, knowledge of the inflammatory response and its biological significance during the lytic EBV cycle remains elusive. Here, we demonstrate that the immediate early transcriptional activator BZLF1 suppresses the proinflammatory factor tumor necrosis factor alpha (TNF-α) by binding to the promoter of TNF-α and preventing NF-κB activation. A BZLF1Δ207-210 mutant with a deletion of 4 amino acids (aa) in the protein-protein binding domain was not able to inhibit the proinflammatory factors TNF-α and gamma interferon (IFN-γ) and reduced viral DNA replication with complete transcriptional activity during EBV lytic gene expression. TNF-α depletion restored the viral replication mediated by BZLF1Δ207-210. Furthermore, a combination of TNF-α- and IFN-γ-neutralizing antibodies recovered BZLF1Δ207-210-mediated viral replication, indicating that BZLF1 attenuates the antiviral response to aid optimal lytic replication primarily through the inhibition of TNF-α and IFN-γ secretion during the lytic cycle. These results suggest that EBV BZLF1 attenuates the proinflammatory responses to facilitate viral replication.IMPORTANCEThe proinflammatory response is an antiviral and anticancer strategy following the complex inflammatory phenotype. Latent Epstein-Barr virus (EBV) infection strongly correlates with an elevated secretion of inflammatory factors in a variety of severe diseases, while the inflammatory responses during the lytic EBV cycle have not been established. Here, we demonstrate that BZLF1 acts as a transcriptional suppressor of the inflammatory factors TNF-α and IFN-γ and confirm that BZLF1-facilitated escape from the TNF-α and IFN-γ response during the EBV lytic life cycle is required for optimal viral replication. This finding implies that the EBV lytic cycle employs a distinct strategy to evade the antiviral inflammatory response.

Contribution of Blastocystishominis subtypes and associated inflammatory factors in development of irritable bowel syndrome

2016 ◽  
Vol 115 (5) ◽  
pp. 2003-2009 ◽  
Author(s):  
Marzieh Azizian ◽  
Gholam Basati ◽  
Ghobad Abangah ◽  
Mohammad Reza Mahmoudi ◽  
Asad Mirzaei
Keyword(s):  
Irritable Bowel Syndrome ◽  
Inflammatory Factors ◽  
Irritable Bowel

scholarly journals Elevated Serum Levels of IL-6 and TNF-α in Patients with Irritable Bowel Syndrome

2019 ◽  
Vol 27 (2) ◽  
pp. 21-29
Author(s):  
Marzieh Azizyan ◽  
Habibolah Turki ◽  
Asad Mirzaei ◽  
◽  
◽  
...  
Keyword(s):  
Irritable Bowel Syndrome ◽  
Elevated Serum ◽  
Serum Levels ◽  
Tnf Α ◽  
Irritable Bowel

scholarly journals Effect of acupuncture combined with Astragalus injection on peripheral blood inflammatory factors in children with diarrhea-predominant irritable bowel syndrome

2019 ◽  
Vol 17 ◽  
pp. 205873921985368 ◽  
Author(s):  
Huimin Xue ◽  
Shan Shao
Keyword(s):  
Irritable Bowel Syndrome ◽  
Acupuncture Therapy ◽  
Peripheral Blood ◽  
Inflammatory Factors ◽  
Control Group ◽  
Therapeutic Effects ◽  
Study Group ◽  
Calcitonin Gene ◽  
Irritable Bowel ◽  
Better Than

The objective of this article is to explore the clinical efficacy of acupuncture therapy of Traditional Chinese Medicine (TCM) combined with Astragalus injection in the treatment of children with diarrhea-predominant irritable bowel syndrome (IBS), and its effects on 5-hydroxytryptamine (5-HT), neuropeptide Y (NPY), and calcitonin gene-related peptide (CGRP) in peripheral blood. A total of 116 children with diarrhea-predominant IBS admitted to our hospital from January 2017 to January 2018 were randomly divided into two groups. The control group was treated with Astragalus injection, while the research group was treated with acupuncture therapy of TCM combined with Astragalus injection. The therapeutic effects, the concentrations of CGRP, NPY, and 5-HT in peripheral blood were compared between the two groups. The therapeutic efficacy of the study group was better than that of the control group ( P < 0.05). The concentrations of CGRP, NPY, and 5-HT in the peripheral blood of the study group were less than those of the control group ( P < 0.05). Acupuncture therapy of TCM combined with Astragalus injection has a satisfactory effect in the treatment of children with diarrhea-predominant IBS, which is worthy of more publicity and application in the clinic.

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