GLORIA

GEOMAR Library Ocean Research Information Access

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Dietary Monounsaturated n-3 and n-6 Long-Chain Polyunsaturated Fatty Acids Affect Cellular Antioxidant Defense System in Rats with Experimental Ulcerative Colitis Induced by Trinitrobenzene Sulfonic Acid (1998)
    Springer
    Digestive diseases and sciences 43 (1998), S. 2676-2687 
    Details
    ISSN: 1573-2568
    Keywords: ANTIOXIDANTS ; EICOSANOIDS ; FATTY ACIDS ; FREE RADICALS ; INFLAMMATORY BOWEL DISEASE ; ULCERATIVE COLITIS ; TRINITROBENZENE SULFONIC ACID
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The intrarectal administration oftrinitrobenzene sulfonic acid in rats induces ulcerativecolitis, which results in histological alterations ofcolonic mucosa, severe modification of the cellularantioxidant defense system, and enhanced production ofinflammatory eicosanoids. This study evaluated theinfluence of different dietary fatty acids, ie,monounsaturated, n-3, and n-3 + n-6 polyunsaturatedfatty acids, on the recovery of the colonic mucosahistological pattern, the cellular antioxidant defensesystem of colon, and PGE2 and LTB4colonic mucosa contents in a model of ulcerative colitisinduced by intrarectal administration of trinitrobenzene sulfonicacid. Administration of dietary n-3 polyunsaturatedfatty acids led to a minimum stenosis score, a higherhistological recovery, lower colon alkaline phosphatase and gamma-glutamyltranspeptidase activities,and lower mucosal levels of PGE2 andLTB4 compared with the other two experimentalgroups. However, glutathione transferase, glutathionereductase, glutathione peroxidase, and catalase activities were lowerin the group treated with n-3 polyunsaturated fattyacids than in the groups fed with either themonounsaturated or the n-6 + n-3 polyunsaturatedenriched diet. We conclude that n-3 polyunsaturatedfatty acids can be administered to prevent inflammationin ulcerative colitis, but they cause a decrease in thecolonic antioxidant defense system, promoting oxidative injury at the site of inflammation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026655311878
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Changes in Plasma and Colonic Mucosa Fatty Acid Profiles in Rats with Ulcerative Colitis Induced by Trinitrobenzene Sulfonic Acid (1998)
    Springer
    Digestive diseases and sciences 43 (1998), S. 2688-2695 
    Details
    ISSN: 1573-2568
    Keywords: COLON ; FATTY ACID ; INFLAMMATORY BOWEL DISEASE ; ULCERATIVE COLITIS ; TRINITROBENZENESULFONIC ACID
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Polyunsaturated fatty acids have a key role inthe pathogenesis of inflammatory bowel disease sincesome of the arachidonic acid-derived eicosanoids havebeen found to be increased in inflamed intestinal mucosa in the acute phase of human disease. Theaim of this study was to prospectively assess plasma andcolon mucosa fatty acid patterns in rats withexperimental ulcerative colitis. Twenty rats weretreated with trinitrobenzene sulfonic acid and 20 withNaCl; two groups were killed after one week and twoafter two weeks to evaluate colon damage. Plasma wasobtained by aortic puncture and colonic mucosa was scraped off and the fatty acid pattern wasdetermined by gas-liquid chromatography. Total,saturated, and monounsaturated plasma fatty acids weresignificantly higher in both periods of ulcerativecolitis as compared to controls. Plasma n-6 fatty acidswere increased after treatment, but no significantchanges were observed concerning to n-3 fatty acids.With regard to colon mucosa, saturated andmonounsaturated fatty acids did not change because of thedisease; however, n-6 fatty acids decreased in the firstweek and increased in the second week and n-3 fattyacids were increased. Changes on the fatty aciddistribution in plasma did not parallel to those of colonicmucosa except for 22:6(n-3). We have also found thatexperimental ulcerative colitis induced bytrinitrobenzene sulfonic acid reproduces many of thefeatures related to changes in plasma and colon mucosafatty acids observed in the human disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026607428716
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Experimental Ulcerative Colitis Impairs Antioxidant Defense System in Rat Intestine (2000)
    Springer
    Digestive diseases and sciences 45 (2000), S. 1820-1827 
    Details
    ISSN: 1573-2568
    Keywords: trinitrobenzenesulfonic acid ; ulcerative colitis ; antioxidant defense system ; eicosanoids ; reactive oxygen species
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Increasing attention has been given recently to the role of free radicals in the pathogenesis of ulcerative colitis, since the inflamed intestine is exposed to oxidative stress generated by infiltrating macrophages and neutrophils within the lamina propia. The overall goal of this study was to evaluate whether experimental ulcerative colitis induces significant changes in the antioxidant defense system in an experimental model induced by the intrarectal administration of 2,4,6-trinitrobenzenesulfonic acid. Twenty rats were treated with 80 mg/kg body weight of trinitrobenzenesulfonic acid and 20 with the same volume of 0.9% NaCl. Rats were killed at one and two weeks after treatment to evaluate colon damage by light and electron transmission microscopy. The degree of tissue injury and inflammation was determined by measuring alkaline phosphatase, γ-glutamyltranspeptidase, and myeloperoxidase activities and prostaglandin E2 and leukotriene B4. Glutathione levels and the activity of the enzymes of the antioxidant defense system were determined. Enzymatic markers of colon injury showed higher activities in rats with ulcerative colitis. Concentrations of prostaglandin E2 and leukotriene B4 were higher in the groups treated for one week with trinitrobenzenesulfonic acid and markers decreased after two weeks of treatment. All antioxidant enzyme activities were higher at one and two weeks after treatment; however, a significant decrease in total glutathione content was also observed. In conclusion, ulcerative colitis induced by trinitrobenzenesulfonic acid damages the intestinal mucosa and is accompanied by a shift in the antioxidant enzyme activities, and low levels of glutathione. This deficiency in glutathione could be a target for new therapies to treat ulcerative colitis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1005565708038
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Experimental Colitis Induced by Trinitrobenzenesulfonic Acid (An Ultrastructural and Histochemical Study) (1999)
    Springer
    Digestive diseases and sciences 44 (1999), S. 2523-2529 
    Details
    ISSN: 1573-2568
    Keywords: INFLAMMATORY BOWEL DISEASE ; TRINITROBENZENESULFONIC ACID ; HISTOLOGY ; ULTRASTRUCTURE
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Inflammatory bowel disease (IBD) of humans is achronic and devastating disease of unknown etiology.Models of acute colitis in animals have been achieved byintrarectal administration of agents such as 2,4,6-trinitrobenzenesulfonic acid (TNBS) intorat colon. This agent induces focal inflammation andalterations in the colon with features similar to thosefound in chronic inflammatory diseases in humans. The aim of this study was to assess the effectof TNBS administration on histological andultrastructural features of the rat colon, especially inareas not affected by transmural inflammation. Also in areas without transmural inflammation, weobserved a significant increase in crypt diameter and inthe number and area of the goblet cells, as well asalterations in the contents of mucin in goblet cells. We conclude that TNBS treatment in rats led tosevere changes in normal architecture of the colon andalso in damaged areas where no direct inflammation wasproduced.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026651408998
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    facet.materialart.
    Unknown
    Outcomes in hepatitis C virus seropositive lymphoma and myeloma patients after autologous stem cell transplantation (2016)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2016-07-07
    Description: Outcomes in hepatitis C virus seropositive lymphoma and myeloma patients after autologous stem cell transplantation Bone Marrow Transplantation 51, 999 (July 2016). doi:10.1038/bmt.2016.28 Authors: A Varma, R M Saliba, H A Torres, A Afrough, C Hosing, I F Khouri, Y Nieto, N D Shah, S Parmar, Q Bashir, S Ahmed, R B Jones, P Kebriaei, A L Olson, E J Shpall, A M Alousi, M H Qazilbash, R E Champlin & U Popat
    Print ISSN: 0268-3369
    Electronic ISSN: 1476-5365
    Topics: Medicine
    Published by Nature Publishing Group (NPG)
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 6
    facet.materialart.
    Unknown
    Genome-wide transcriptome analysis identifies novel gene signatures implicated in human chronic liver disease (2013)
    The American Physiological Society (APS)
    Details
    Publication Date: 2013-09-06
    Description: The molecular mechanisms behind human liver disease progression to cirrhosis remain elusive. Nuclear receptor small heterodimer partner (SHP/ Nr0b2 ) is a hepatic tumor suppressor and a critical regulator of liver function. SHP expression is diminished in human cirrhotic livers, suggesting a regulatory role in human liver diseases. The goal of this study was to identify novel SHP-regulated genes that are involved in the development and progression of chronic liver disease. To achieve this, we conducted the first comprehensive RNA sequencing (RNA-seq) analysis of Shp –/– mice, compared the results with human hepatitis C cirrhosis RNA-seq and nonalcoholic steatohepatitis (NASH) microarray datasets, and verified novel results in human liver biospecimens. This approach revealed new gene signatures associated with chronic liver disease and regulated by SHP. Several genes were selected for validation of physiological relevance based on their marked upregulation, novelty with regard to liver function, and involvement in gene pathways related to liver disease. These genes include peptidoglycan recognition protein 2, dual specific phosphatase-4, tetraspanin 4, thrombospondin 1, and SPARC-related modular calcium binding protein-2, which were validated by qPCR analysis of 126 human liver specimens, including steatosis, fibrosis, and NASH, alcohol and hepatitis C cirrhosis, and in mouse models of liver inflammation and injury. This RNA-seq analysis identifies new genes that are regulated by the nuclear receptor SHP and implicated in the molecular pathogenesis of human chronic liver diseases. The results provide valuable transcriptome information for characterizing mechanisms of these diseases.
    Print ISSN: 0193-1857
    Electronic ISSN: 1522-1547
    Topics: Medicine
    Published by The American Physiological Society (APS)
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 7
    facet.materialart.
    Unknown
    Milk osteopontin, a nutritional approach to prevent alcohol-induced liver injury (2013)
    The American Physiological Society (APS)
    Details
    Publication Date: 2013-05-16
    Description: Alcohol consumption is a leading cause of liver disease worldwide; thus, there is an urgent need to develop novel therapeutic interventions. Key events for the onset and progression of alcoholic liver disease result in part from the gut-to-liver interaction. Osteopontin is a cytokine present at high concentration in human milk, umbilical cord, and infants' plasma with beneficial potential. We hypothesized that dietary administration of milk osteopontin could prevent alcohol-induced liver injury perhaps by maintaining gut integrity and averting hepatic inflammation and steatosis. Wild-type mice were fed either the control or the ethanol Lieber-DeCarli diets alone or in combination with milk osteopontin for 3 wk, and parameters of gut and liver damage were measured. Milk osteopontin protected the stomach and the gut by increasing gland height, crypt cell plus enterocyte proliferation, and mucin content in addition to lowering macrophages, plasmacytes, lymphocytes, and neutrophils in the mucosa and submucosa in alcohol-fed mice. Milk osteopontin targeted the gut-liver axis, preserving the expression of tight-junction proteins in alcohol-fed mice thus maintaining intestinal integrity and permeability. There was protection from liver injury since transaminases, the activity scores, triglyceride levels, neutrophil infiltration, 3-nitrotyrosine residues, lipid peroxidation end products, translocation of gram-negative bacteria, lipopolysaccharide levels, and tumor necrosis factor-α were lower in cotreated than in ethanol-fed mice. Furthermore, milk osteopontin diminished ethanol-mediated liver injury in OPN knockout mice. Milk osteopontin could be a simple effective nutritional therapeutic strategy to prevent alcohol hepatotoxicity due, among others, to gut protective, anti-inflammatory, and anti-steatotic actions.
    Print ISSN: 0193-1857
    Electronic ISSN: 1522-1547
    Topics: Medicine
    Published by The American Physiological Society (APS)
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 8
    facet.materialart.
    Unknown
    HMGB1 and ALD [Metabolism] (2014)
    The American Society for Biochemistry and Molecular Biology (ASBMB)
    Details
    Publication Date: 2014-08-15
    Description: Growing clinical and experimental evidence suggests that sterile inflammation contributes to alcoholic liver disease (ALD). High mobility group box-1 (HMGB1) is highly induced during liver injury; however, a link between this alarmin and ALD has not been established. Thus, the aim of this work was to determine whether HMGB1 contributes to the pathogenesis of ALD. Liver biopsies from patients with ALD showed a robust increase in HMGB1 expression and translocation, which correlated with disease stage, compared with healthy explants. Similar findings were observed in chronic ethanol-fed wild-type (WT) mice. Using primary cell culture, we validated the ability of hepatocytes from ethanol-fed mice to secrete a large amount of HMGB1. Secretion was time- and dose-dependent and responsive to prooxidants and antioxidants. Selective ablation of Hmgb1 in hepatocytes protected mice from alcohol-induced liver injury due to increased carnitine palmitoyltransferase-1, phosphorylated 5′AMP-activated protein kinase-α, and phosphorylated peroxisome proliferator-activated receptor-α expression along with elevated LDL plus VLDL export. Native and post-translationally modified HMGB1 were detected in humans and mice with ALD. In liver and serum from control mice and in serum from healthy volunteers, the lysine residues within the peptides containing nuclear localization signals (NLSs) 1 and 2 were non-acetylated, and all cysteine residues were reduced. However, in livers from ethanol-fed mice, in addition to all thiol/non-acetylated isoforms of HMGB1, we observed acetylated NLS1 and NLS2, a unique phosphorylation site in serine 35, and an increase in oxidation of HMGB1 to the disulfide isoform. In serum from ethanol-fed mice and from patients with ALD, there was disulfide-bonded hyperacetylated HMGB1, disulfide-bonded non-acetylated HMGB1, and HMGB1 phosphorylated in serine 35. Hepatocytes appeared to be a major source of these HMGB1 isoforms. Thus, hepatocyte HMGB1 participates in the pathogenesis of ALD and undergoes post-translational modifications (PTMs) that could condition its toxic effects.
    Print ISSN: 0021-9258
    Electronic ISSN: 1083-351X
    Topics: Biology , Chemistry and Pharmacology
    Published by The American Society for Biochemistry and Molecular Biology (ASBMB)
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 9
    facet.materialart.
    Unknown
    Cu/Zn superoxide dismutase (SOD1) induction is implicated in the antioxidative and antiviral activity of acetylsalicylic acid in HCV-expressing cells (2012)
    The American Physiological Society (APS)
    Details
    Publication Date: 2012-06-02
    Description: We evaluated the participation of oxidative stress in the negative regulation of hepatitis C virus (HCV)-RNA induced by acetylsalicylic acid (ASA). We used the HCV subgenomic replicon cell system that stably expresses HCV-nonstructural proteins (Huh7 HCV replicon cells) and the parental cell line. Cells were exposed to 4 mM ASA at different times (12–72 h), and pyrrolidine dithiocarbamate (PDTC) was used as an antioxidant control. Reactive oxygen species (ROS) production, oxidized protein levels, cytosolic superoxide dismutase (Cu/Zn-SOD), and glutathione peroxidase (GPx) activity were measured to evaluate oxidative stress. In addition, viral RNA and prostaglandin (PGE 2 ) levels were determined. We observed that ASA treatment decreased ROS production and oxidized protein levels in a time-dependent fashion in both parental and HCV replicon cells with a greater extent in the latter. Similar results were found with PDTC exposure. Average GPx activity was decreased, whereas a striking increase was observed in average cytosolic SOD activity at 48 and 72 h in both cells exposed to ASA, compared with untreated cells. HCV replicon cells showed higher levels of Cu/Zn-SOD expression (mRNA and protein) with ASA treatment (48 and 72 h), whereas NS5A protein levels showed decreased expression. In addition, we found that inhibition of SOD1 expression reversed the effect of ASA. Interestingly, PDTC downregulated HCV-RNA expression (55%) and PGE 2 (60%) levels, imitating ASA exposure. These results suggest that ASA treatment could reduce cellular oxidative stress markers and modify Cu/Zn-SOD expression, a phenomenon that may contribute to the mechanisms involved in HCV downregulation.
    Print ISSN: 0193-1857
    Electronic ISSN: 1522-1547
    Topics: Medicine
    Published by The American Physiological Society (APS)
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 10
    facet.materialart.
    Unknown
    Arachidonic acid stimulates TNF{alpha} production in Kupffer cells via a reactive oxygen species-pERK1/2-Egr1-dependent mechanism (2012)
    The American Physiological Society (APS)
    Details
    Publication Date: 2012-07-16
    Description: Kupffer cells are a key source of mediators of alcohol-induced liver damage such as reactive oxygen species, chemokines, growth factors, and eicosanoids. Since diets rich in polyunsaturated fatty acids are a requirement for the development of alcoholic liver disease, we hypothesized that polyunsaturated fatty acids could synergize with ethanol to promote Kupffer cell activation and TNFα production, hence, contributing to liver injury. Primary Kupffer cells from control and from ethanol-fed rats incubated with arachidonic acid showed similar proliferation rates than nontreated cells; however, arachidonic acid induced phenotypic changes, lipid peroxidation, hydroperoxides, and superoxide radical generation. Similar effects occurred in human Kupffer cells. These events were greater in Kupffer cells from ethanol-fed rats, and antioxidants and inhibitors of arachidonic acid metabolism prevented them. Arachidonic acid treatment increased NADPH oxidase activity. Inhibitors of NADPH oxidase and of arachidonic acid metabolism partially prevented the increase in oxidant stress. Upon arachidonic acid stimulation, there was a rapid and sustained increase in TNFα, which was greater in Kupffer cells from ethanol-fed rats than in Kupffer cells from control rats. Arachidonic acid induced ERK1/2 phosphorylation and nuclear translocation of early growth response-1 (Egr1), and ethanol synergized with arachidonic acid to promote this effect. PD98059, a mitogen extracellular kinase 1/2 inhibitor, and curcumin, an Egr1 inhibitor, blocked the arachidonic acid-mediated upregulation of TNFα in Kupffer cells. This study unveils the mechanism whereby arachidonic acid and ethanol increase TNFα production in Kupffer cells, thus contributing to alcoholic liver disease.
    Print ISSN: 0193-1857
    Electronic ISSN: 1522-1547
    Topics: Medicine
    Published by The American Physiological Society (APS)
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...