scholarly journals The effect of Hericium erinaceum on the prevention of chemically induced experimental colitis in rats

2020 ◽  
Author(s):  
Ali Durmus ◽  
Ilgim Durmus ◽  
Omer Bender ◽  
Oguzhan Karatepe
Keyword(s):  
Experimental Colitis ◽  
Chemically Induced ◽  
Hericium Erinaceum

scholarly journals Gasdermin D in macrophages restrains colitis by controlling cGAS-mediated inflammation

2020 ◽  
Vol 6 (21) ◽  
pp. eaaz6717 ◽  
Author(s):  
Chunmei Ma ◽  
Dongxue Yang ◽  
Bingwei Wang ◽  
Chunyan Wu ◽  
Yuqing Wu ◽  
...  
Keyword(s):  
Antimicrobial Peptides ◽  
Cyclic Gmp ◽  
Intestinal Inflammation ◽  
Experimental Colitis ◽  
Underlying Mechanism ◽  
Negative Regulator ◽  
Chemically Induced ◽  
Mechanistic Basis ◽  
Functional Relevance ◽  
Deficient Mice

The functional relevance and mechanistic basis of the effects of the pyroptosis executioner Gasdermin D (GSDMD) on colitis remain unclear. In this study, we observed that GSDMD protein was activated during intestinal inflammation in a model of chemically induced colitis. GSDMD deficiency exacerbated experimental colitis independent of changes in the microbiota and without affecting the production of antimicrobial peptides. GSDMD deficiency in macrophages, but not epithelial cells, was sufficient to drive this exacerbated experimental colitis. We further demonstrate that GSDMD functions in macrophages as a negative regulator to control cyclic GMP–AMP synthase (cGAS)–dependent inflammation, thereby protecting against colitis. Moreover, the administration of cGAS inhibitor can rescue the colitogenic phenotype in GSDMD-deficient mice. Collectively, these findings provide the first demonstration of GSDMD’s role in controlling colitis and a detailed delineation of the underlying mechanism.

scholarly journals Hyaluronan Synthase 3 Null Mice Exhibit Decreased Intestinal Inflammation and Tissue Damage in the DSS-Induced Colitis Model

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Sean P. Kessler ◽  
Dana R. Obery ◽  
Carol de la Motte
Keyword(s):  
Intestinal Inflammation ◽  
Inflammatory Diseases ◽  
Experimental Colitis ◽  
Hyaluronan Synthase ◽  
Wild Type ◽  
Colon Tissue ◽  
Dss Colitis ◽  
Chemically Induced ◽  
Inflammatory Bowel ◽  
Colitis Model

Hyaluronan (HA) overproduction is a hallmark of multiple inflammatory diseases, including inflammatory bowel disease (IBD). Hyaluronan can act as a leukocyte recruitment molecule and in the most common mouse model of intestinal inflammation, the chemically induced dextran sodium sulfate (DSS) experimental colitis model, we previously determined that changes in colon distribution of HA occur before inflammation. Therefore, we hypothesized that, during a pathologic challenge, HA promotes inflammation. In this study, we tested the progression of inflammation in mice null for the hyaluronan synthase genes (HAS1, HAS3, or both HAS1 and HAS3) in the DSS-colitis model. Our data demonstrate that both the HAS1/HAS3 double and the HAS3 null mice are protected from colitis, compared to wild-type and HAS1 null mice, as determined by measurement of weight loss, disease activity, serum IL-6 levels, histologic scoring, and immunohistochemistry. Most notable is the dramatic increase in submucosal microvasculature, hyaluronan deposition, and leukocyte infiltration in the inflamed colon tissue of wild-type and HAS1 null mice. Our data suggest, HAS3 plays a crucial role in driving gut inflammation. Developing a temporary targeted therapeutic intervention of HAS3 expression or function in the microcirculation may emerge as a desirable strategy toward tempering colitis in patients undergoing flares of IBD.

Enteral diets enriched with medium-chain triglycerides and N-3 fatty acids prevent chemically induced experimental colitis in rats

2010 ◽  
Vol 156 (5) ◽  
pp. 282-291 ◽  
Author(s):  
Hiroshi Kono ◽  
Hideki Fujii ◽  
Masahito Ogiku ◽  
Masato Tsuchiya ◽  
Kenichi Ishii ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Experimental Colitis ◽  
Medium Chain Triglycerides ◽  
Medium Chain ◽  
Chemically Induced

scholarly journals Essential role for mast cell tryptase in acute experimental colitis

2010 ◽  
Vol 108 (1) ◽  
pp. 290-295 ◽  
Author(s):  
Matthew J. Hamilton ◽  
Mark J. Sinnamon ◽  
Gregory D. Lyng ◽  
Jonathan N. Glickman ◽  
Xueli Wang ◽  
...  
Keyword(s):  
Weight Loss ◽  
Mast Cell ◽  
Experimental Colitis ◽  
Distal Colon ◽  
Trinitrobenzene Sulfonic Acid ◽  
Chemically Induced ◽  
Inflammatory Bowel ◽  
Proinflammatory Role ◽  
Mouse Mast Cell ◽  
Microarray Analyses

Patients with inflammatory bowel disease (IBD) have increased numbers of human tryptase-β (hTryptase-β)-positive mast cells (MCs) in the gastrointestinal tract. The amino acid sequence of mouse mast cell protease (mMCP)-6 is most similar to that of hTryptase-β. We therefore hypothesized that this mMCP, or the related tryptase mMCP-7, might have a prominent proinflammatory role in experimental colitis. The dextran sodium sulfate (DSS) and trinitrobenzene sulfonic acid (TNBS) colitis models were used to evaluate the differences between C57BL/6 (B6) mouse lines that differ in their expression of mMCP-6 and mMCP-7 with regard to weight loss, colon histopathology, and endoscopy scores. Microarray analyses were performed, and confirmatory real-time PCR, ELISA, and/or immunohistochemical analyses were carried out on a number of differentially expressed cytokines, chemokines, and matrix metalloproteinases (MMPs). The mMCP-6–null mice that had been exposed to DSS had significantly less weight loss as well as significantly lower pathology and endoscopy scores than similarly treated mMCP-6–expressing mice. This difference in colitis severity was confirmed endoscopically in the TNBS-treated mice. Evaluation of the distal colon segments revealed that numerous proinflammatory cytokines, chemokines that preferentially attract neutrophils, and MMPs that participate in the remodeling of the ECM were all markedly increased in the colons of DSS-treated WT mice relative to untreated WT mice and DSS-treated mMCP-6–null mice. Collectively, our data show that mMCP-6 (but not mMCP-7) is an essential MC-restricted mediator in chemically induced colitis and that this tryptase acts upstream of many of the factors implicated in IBD.

Dietary medium-chain triglycerides prevent chemically induced experimental colitis in rats

2010 ◽  
Vol 155 (3) ◽  
pp. 131-141 ◽  
Author(s):  
Hiroshi Kono ◽  
Hideki Fujii ◽  
Kenichi Ishii ◽  
Naohiro Hosomura ◽  
Masahito Ogiku
Keyword(s):  
Experimental Colitis ◽  
Medium Chain Triglycerides ◽  
Medium Chain ◽  
Chemically Induced

scholarly journals The effect of progesterone in the prevention of the chemically induced experimental colitis in rats

2012 ◽  
Vol 27 (1) ◽  
pp. 23-29 ◽  
Author(s):  
Oguzhan Karatepe ◽  
Merih Altiok ◽  
Muharrem Battal ◽  
Gulcin Kamali ◽  
Ahu Kemik ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Experimental Colitis ◽  
Control Group ◽  
Albino Rats ◽  
Trinitrobenzene Sulfonic Acid ◽  
Colon Tissue ◽  
Chemically Induced ◽  
Group 3 ◽  
Group 2 ◽  
Wistar Albino Rats

PURPOSE: To study the effects of progesterone on an experimental colitis model. METHODS: Wistar albino rats were treated subcutaneously with 2mg/kg once a day during seven days Colitis was induced by intrarectal administration of 5mg trinitrobenzene sulfonic acid (TNBS). Disease activities, macroscopic and microscopic scores were evaluated. To determine the response provoked by progesterone we measured Colonic malondialdehyde (MDA), TNF alfa, IL-6 and Nitric oxide (NO) levels in addition to the MPO (Myeloperoxidase) and caspase-3 activities. RESULTS: Progesterone ameliorated significantly the macroscopic and microscopic scores. TNBS-induced colitis significantly increased the colonic MDA levels and caspase-3 activities in group 2 in comparison to the control group. The results of the study revealed a decline in MDA, NO, IL6 and TNF-α levels in the colon tissue and in blood due to progesterone therapy in group 3 when compared to the group 2, a significant improvement. Progesterone treatment was associated with decreased MDA, MPO, TNF alfa and caspase-3 activity. CONCLUSION: Progesterone therapy decreased oxidative damage in the colonic mucosa.

Interleukin 19 reduces inflammation in chemically induced experimental colitis

2015 ◽  
Vol 29 (2) ◽  
pp. 468-475 ◽  
Author(s):  
Yukiko Matsuo ◽  
Yasu-Taka Azuma ◽  
Mitsuru Kuwamura ◽  
Nobuyuki Kuramoto ◽  
Kazuhiro Nishiyama ◽  
...  
Keyword(s):  
Experimental Colitis ◽  
Chemically Induced

Biological and Surface Properties of C-Type Virus Particles Produced by Novikoff Ascites Hepatoma Cells

1977 ◽  
Vol 35 ◽  
pp. 388-389
Author(s):  
D.C. Hixson ◽  
J.C. Chan ◽  
J.M. Bowen ◽  
E.F. Walborg
Keyword(s):  
Surface Properties ◽  
Ricinus Communis ◽  
Rat Kidney ◽  
Leukemia Virus ◽  
Viral Envelope ◽  
Virus Particles ◽  
Chemically Induced ◽  
Sarcoma Virus ◽  
Hepatocarcinoma Cells ◽  
Type C

Several years ago Karasaki (1) reported the production of type C virus particles by Novikoff ascites hepatocarcinoma cells. More recently, Weinstein (2) has reported the presence of type C virus particles in cell cultures derived from transplantable and primary hepatocellular carcinomas. To date, the biological function of these virus and their significance in chemically induced hepatocarcinogenesis are unknown. The present studies were initiated to determine a possible role for type C virus particles in chemically induced hepatocarcinogenesis. This communication describes results of studies on the biological and surface properties of type C virus associated with Novikoff hepatocarcinoma cells.Ecotropic and xenotropic murine leukemia virus (MuLV) activity in ascitic fluid of Novikoff tumor-bearing rats was assayed in murine sarcoma virus transformed S+L- mouse cells and S+L- mink cells, respectively. The presence of sarcoma virus activity was assayed in non-virus-producing normal rat kidney (NRK) cells. Ferritin conjugates of concanavalin A (Fer-Con wheat germ agglutinin (Fer-WGA), and Ricinus communis agglutinins I and II (Fer-RCAI and Fer-RCAII) were used to probe the structure and topography of saccharide determinants present on the viral envelope.

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