scholarly journals Protective Effects of Aminooxyacetic Acid on Colitis Induced in Mice with Dextran Sulfate Sodium

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Wenyang Li ◽  
Jianghong Yu ◽  
Bohan Jin ◽  
Huilu Zhang ◽  
Jun Zhang
Keyword(s):  
Pyridoxal Phosphate ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Aminooxyacetic Acid ◽  
Intermediate Filament Protein ◽  
Macrophage Phenotype ◽  
Short Term Treatment ◽  
M1 Macrophage ◽  
Tnf Α ◽  
Cell Proliferation Inhibition

As a known inhibitor of pyridoxal phosphate-dependent transaminase glutamic-oxaloacetic transaminase 1 (GOT1), aminooxyacetic acid (AOAA) has been pointed out to have potential pharmacological effects in antiepileptic, anticonvulsant, antibacterial, cancer cell proliferation inhibition, and acute myocardial infarction (MI) relief. However, its role in inflammatory bowel disease (IBD) has not been reported. Through the in vivo experiment of dextran sulfate sodium- (DSS-) induced colitis in mice, it was found that AOAA significantly attenuated the symptoms, signs, and pathological changes of colitis. In addition, AOAA treatment prevented gut barrier damages by enhancing the expression of zona occludens- (ZO-) 1, occludin, claudin-1, and E-cadherin and recovering the upregulation of the most abundant intermediate filament protein (vimentin). Moreover, the release of interleukin- (IL-) 1β, IL-6, and tumour necrosis factor- (TNF-) α was suppressed, yet the level of IL-10 was upregulated by AOAA treatment compared to the model group. Furthermore, it was shown that AOAA administration boosted M2-like phenotype and effectively reduced M1 macrophage phenotype in the lamina propria of mouse colonic epithelium. Similarly, the effect of AOAA was verified in vitro. AOAA effectively inhibited the classically activated M1 macrophage phenotype and proinflammatory cytokine (IL-1β, TNF-α, and IL-6) expression induced by lipopolysaccharide (LPS) and promoted M2-like phenotype. Collectively, this study reveals for the first time that short-term treatment of AOAA can significantly alleviate DSS-induced acute colitis by regulating intestinal barrier function and macrophage polarization, which provides a theoretical basis for the potential use of AOAA in the treatment of IBD.

Oat β-glucan ameliorates dextran sulfate sodium (DSS)-induced ulcerative colitis in mice

2015 ◽  
Vol 6 (11) ◽  
pp. 3454-3463 ◽  
Author(s):  
Bo Liu ◽  
Qinlu Lin ◽  
Tao Yang ◽  
Linna Zeng ◽  
Limin Shi ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Oral Administration ◽  
Inflammatory Cytokines ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Tnf Α

Oral administration of oat β-glucan ameliorates DSS induced colitis in mice by decreasing the expression of inflammatory cytokines TNF-α, IL-1β, IL-6 and iNOS.

scholarly journals Exposure to the Harmful Algal Bloom (HAB) Toxin Microcystin-LR (MC-LR) Prolongs and Increases Severity of Dextran Sulfate Sodium (DSS)-Induced Colitis

Toxins ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 371 ◽  
Author(s):  
Robin C. Su ◽  
Thomas M. Blomquist ◽  
Andrew L. Kleinhenz ◽  
Fatimah K. Khalaf ◽  
Prabhatchandra Dube ◽  
...  
Keyword(s):  
Weight Loss ◽  
Algal Blooms ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Harmful Algal Bloom ◽  
Tnf Α ◽  
Environmental Toxin ◽  
Genetic And Environmental Factors ◽  
The Impact ◽  
Bloody Stools

Inflammatory Bowel Disease (IBD) represents a collection of gastrointestinal disorders resulting from genetic and environmental factors. Microcystin-leucine arginine (MC-LR) is a toxin produced by cyanobacteria during algal blooms and demonstrates bioaccumulation in the intestinal tract following ingestion. Little is known about the impact of MC-LR ingestion in individuals with IBD. In this study, we sought to investigate MC-LR’s effects in a dextran sulfate sodium (DSS)-induced colitis model. Mice were separated into four groups: (a) water only (control), (b) DSS followed by water (DSS), (c) water followed by MC-LR (MC-LR), and (d) DSS followed by MC-LR (DSS + MC-LR). DSS resulted in weight loss, splenomegaly, and severe colitis marked by transmural acute inflammation, ulceration, shortened colon length, and bloody stools. DSS + MC-LR mice experienced prolonged weight loss and bloody stools, increased ulceration of colonic mucosa, and shorter colon length as compared with DSS mice. DSS + MC-LR also resulted in greater increases in pro-inflammatory transcripts within colonic tissue (TNF-α, IL-1β, CD40, MCP-1) and the pro-fibrotic marker, PAI-1, as compared to DSS-only ingestion. These findings demonstrate that MC-LR exposure not only prolongs, but also worsens the severity of pre-existing colitis, strengthening evidence of MC-LR as an under-recognized environmental toxin in vulnerable populations, such as those with IBD.

Xanthoangelol Isolated from Angelica keiskei Roots Prevents Dextran Sulfate Sodium-Treated Colitis in Mice

2020 ◽  
Vol 10 (5) ◽  
pp. 655-663
Author(s):  
Yoshiyuki Kimura ◽  
Kimye Baba
Keyword(s):  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Activity Index ◽  
Gastrointestinal Diseases ◽  
Gastric Ulcers ◽  
Eosinophil Infiltration ◽  
Full Blood Count ◽  
Therapeutic Effects ◽  
Tnf Α ◽  
Angelica Keiskei

Background: The therapeutic effects of a number of natural products on Inflammatory Bowel Disease (IBD) have recently been examined in detail. The whole herb and roots of Angelica keiskei (Umblliferae) have traditionally been used as a diuretic, to treat gastrointestinal diseases such as gastric ulcers and diarrhea in Japan. Objectives: The present study was performed to investigate the effects of xanthoangelol, a major chalcone of Angelica keiskei roots, on diarrhea and inflammation in the large intestine of IBD model mice. Methods: Xanthoangelol (10 & 25 mg/kg) was orally administered to mice with 3% Dextran Sulfate Sodium (DSS)-induced colitis. Blood samples were collected during the experimental period, subjected to a full blood count test, and colonic cytokine and chemokine levels were measured. Results: Xanthoangelol (25 mg/kg) reduced the Disease Activity Index (DAI) of colitis. It also attenuated DSS-induced reductions in red blood cell and platelet counts as well as Hb and Ht levels. A histological examination of the colon using direct fast scarlet staining showed that xanthoangelol prevented DSS-induced mucosal ulceration and eosinophil infiltration. Xanthoangelol also reduced DSS-induced increases in colonic MCP-1, IL-1β, and TNF-α levels. Conclusions: Xanthoangelol reduced DSS-induced increases in colonic IL-1β, TNF-α, and MCP-1 levels and prevented eosinophil infiltration, which supports its potential as a treatment for IBD.

scholarly journals Cinobufacini Ameliorates Dextran Sulfate Sodium–Induced Colitis in Mice through Inhibiting M1 Macrophage Polarization

2019 ◽  
Vol 368 (3) ◽  
pp. 391-400 ◽  
Author(s):  
Si-wei Wang ◽  
Yong-feng Bai ◽  
Yuan-yuan Weng ◽  
Xue-yu Fan ◽  
Hui Huang ◽  
...  
Keyword(s):  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Macrophage Polarization ◽  
M1 Macrophage

scholarly journals TSG-6 in extracellular vesicles from canine mesenchymal stem/stromal is a major factor in relieving DSS-induced colitis

2019 ◽  
Author(s):  
Ju-Hyun An ◽  
Woo-Jin Song ◽  
Qiang Li ◽  
Min-Ok Ryu ◽  
A-Ryung Nam ◽  
...  
Keyword(s):  
Extracellular Vesicles ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Qrt Pcr ◽  
Tnf Α ◽  
Key Factor ◽  
Ifn Γ ◽  
Underlying Mechanisms ◽  
Factor Α ◽  
Necrosis Factor

AbstractMesenchymal stem/stromal cell (MSC)-derived extracellular vesicles (EV) have been reported to be beneficial against dextran sulfate sodium (DSS)-induced colitis in mice. However, the underlying mechanisms have not been fully elucidated. We hypothesize that the tumor necrosis factor-α-stimulated gene/protein 6 (TSG-6) in EVs is a key factor influencing the alleviation of colitis symptoms. DSS-induced colitis mice (C57BL/6, male, n = 6-8/group) were intraperitoneally administered EVs (100 ug/mice) on day 1, 3, and 5; colon tissues were collected on day 10 for histopathological, qRT-PCR, western blot, and immunofluorescence analyses. In mice injected with EV, inflammation was alleviated. Indeed, EVs regulated the levels of pro- and anti-inflammatory cytokines, such as TNF-α, IL-1β, IFN-γ, IL-6, and IL-10 in inflamed colons. However, when injected with TSG-6 depleted EV, the degree of inflammatory relief was reduced. Furthermore, TSG-6 in EVs plays a key role in increasing regulatory T cells (Tregs) in the colon. In conclusion, this study shows that TSG-6 in EVs is a major factor in the relief of DSS-induced colitis, by increasing the number of Tregs in the colon.

scholarly journals In Vitro and Ex Vivo Effects of Silymarin Derivatives on Proinflammatory Cytokine Secretion Using a Murine Colonic Strip Model

2018 ◽  
Vol 5 (02) ◽  
pp. e55-e60
Author(s):  
Leo Fitzpatrick ◽  
Ella Mokrushin ◽  
George Talbott ◽  
Tibebe Woldermariam
Keyword(s):  
Cell Lines ◽  
Proinflammatory Cytokine ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Ex Vivo ◽  
Cytokine Secretion ◽  
Raw 264.7 ◽  
Tnf Α ◽  
Anti Inflammatory

AbstractSilymarin has anti-inflammatory properties and documented anti-colitis activity. Our prior study determined that in vitro treatment with certain extracted fractions of silymarin inhibited stimulated proinflammatory cytokine secretion from cell lines relevant to colitis. In this study, colitis was induced in mice by giving dextran sulfate sodium drinking water for 6 days. The ex vivo effects of crude silymarin extract, two different silymarin fractions, as well as commercially derived silibinin and isosilibinin were examined by determining the secretion of MIP-2, TNF-α, and IL-17 in cell culture media from colonic strips. Further, the effects of silymarin-derived treatments on IL-8 and TNF-α secretion induced by the colitis supernatant was characterized with HT-29 colonic epithelial and RAW 264.7 macrophage cell lines. Prominent inhibition of MIP-2 and TNF-α secretion from colonic strips of mice with/without dextran sulfate sodium-induced colitis was observed with various silymarin treatments. Further, inhibition of dual (IL-23+IL-1β) cytokine-stimulated secretion of IL-17 from colonic strips of mice was found with certain silymarin treatments. Significant attenuation of TNF-α secretion from colitis supernatant-stimulated RAW 264.7 cells was observed for crude silymarin extract and isosilibinin treatments. Finally, inhibition of IL-8 secretion from the colitis supernatant-stimulated HT29 colonic epithelial cell line was found with isosilibinin. These results contribute to the identification of silymarin-derived flavonoligans with optimal anti-inflammatory properties for further testing in colitis models.

scholarly journals P0145MESENCHYMAL STEM CELLS PROTECT RENAL TUBULAR CELLS VIA TSG-6 REGULATED MACROPHAGE FUNCTION AND PHENOTYPE SWITCHING

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Yu Zhao ◽  
Xiao liang Zhang ◽  
Bicheng Liu ◽  
Lilach Lerman
Keyword(s):  
Macrophage Phenotype ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
M1 Macrophage ◽  
Tnf Α ◽  
Immunomodulatory Properties ◽  
And Migration ◽  
Renal Tubular

Abstract Background and Aims Tumor necrosis factor-α-induced gene/protein (TSG)-6 is a key factor influencing mesenchymal stem cells (MSCs) immunomodulatory properties, but its renoprotective efficacy is unknown. Using a novel swine model of renal artery stenosis (RAS) complicated by metabolic syndrome (Mets), we assessed the therapeutic effects of adipose tissue-derived MSCs-produced TSG-6 and mechanisms underlying the immunomodulatory properties of MSCs. Method Five groups of pigs (n=6 each) were studied after 16 weeks of diet-induced Mets and unilateral RAS (Mets+RAS), either untreated or treated 4 weeks earlier with a single intra-renal delivery of autologous posrcine adipose tissue-derived MSCs (pMSC). Lean, Mets, and RAS shams served as controls. We studied renal function in vivo (using CT imaging) and kidney histopathology and macrophage phenotype ex vivo. In vitro, TSG-6 levels were measured in conditioned media of human MSCs (hMSCs) incubated with or without TNF-α. Additionally, levels of the tubular injury marker LDH were measured in conditioned media after co-culturing macrophages with injured HK-2 cells (achieved by TNF-α and antimycin-A, AMA) with or without addition of TSG-6. The effects of TSG-6 on macrophage phenotype (M1/M2), adhesion, and migration capability were determined. Results Mets+RAS pigs showed increased renal M1 macrophages and renal vein TNF-α levels. After p-MSCs delivery, renal vein TSG-6 increased and TNF-α decreased, M1 macrophage switched to M2 (Fig. A),, renal function improved, and fibrosis alleviated. In vitro, TNF-α increased TSG-6 secretion by h-MSCs. TSG-6 decreased LDH release from injured HK-2, induced a macrophage phenotypic switch from M1 to M2 (Fig. B), and reduced M1 macrophage adhesion and migration (Fig. C). Conclusion TNF-α-induced TSG-6 release from MSCs in vivo and in vitro may decrease renal tubular cells injury, which is associated with and may be at least in part mediated by regulating macrophage function and phenotype.

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