Increase in tumor necrosis factor-alpha production linked to the toxicity of indomethacin for the rat small intestine.
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Multiple NSAID-induced hits injure the small intestine: underlying mechanisms and novel strategiesNSAID-induced acute phase response is due to increased intestinal permeability and characterized by early and consistent alterations in hepatic gene expressionGlucagon-like peptide 2 decreases mortality and reduces the severity of indomethacin-induced murine enteritisAnti-Ulcer Efficacy of Soluble Epoxide Hydrolase Inhibitor TPPU on Diclofenac-Induced Intestinal UlcersLack of effects of acemetacin on signalling pathways for leukocyte adherence may explain its gastrointestinal safety.Antiinflammatory and neuroprotective actions of COX2 inhibitors in the injured brain.The microbiota-derived metabolite indole decreases mucosal inflammation and injury in a murine model of NSAID enteropathy.Potent analgesic effects of a store-operated calcium channel inhibitor.Review: systemic inflammation and Alzheimer's disease.Mechanisms, prevention and clinical implications of nonsteroidal anti-inflammatory drug-enteropathy.Role of non-steroidal anti-inflammatory drugs on intestinal permeability and nonalcoholic fatty liver disease.Rebamipide protects small intestinal mucosal injuries caused by indomethacin by modulating intestinal microbiota and the gene expression in intestinal mucosa in a rat model.The non-invasive exfoliated transcriptome (exfoliome) reflects the tissue-level transcriptome in a mouse model of NSAID enteropathy.Neutrophil migration into indomethacin induced rat small intestinal injury is CD11a/CD18 and CD11b/CD18 co-dependent.Role of cannabinoid CB1 receptors and tumor necrosis factor-alpha in the gut and systemic anti-inflammatory activity of SR 141716 (rimonabant) in rodents.Lack of small intestinal ulcerogenecity of nitric oxide-releasing indomethacin, NCX-530, in rats.Effects of anti-tumour necrosis factor, interleukin-10 and antibiotic therapy in the indometacin-induced bowel inflammation rat model.Non-steroidal anti-inflammatory drug-induced enteropathy.Pharmacological inhibition of soluble epoxide hydrolase or genetic deletion reduces diclofenac-induced gastric ulcers.Indomethacin-induced small intestinal injury is ameliorated by cilostazol, a specific PDE-3 inhibitor
P2860
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P2860
Increase in tumor necrosis factor-alpha production linked to the toxicity of indomethacin for the rat small intestine.
description
1998 nî lūn-bûn
@nan
1998 թուականի Օգոստոսին հրատարակուած գիտական յօդուած
@hyw
1998 թվականի օգոստոսին հրատարակված գիտական հոդված
@hy
1998年の論文
@ja
1998年論文
@yue
1998年論文
@zh-hant
1998年論文
@zh-hk
1998年論文
@zh-mo
1998年論文
@zh-tw
1998年论文
@wuu
name
Increase in tumor necrosis fac ...... n for the rat small intestine.
@ast
Increase in tumor necrosis fac ...... n for the rat small intestine.
@en
type
label
Increase in tumor necrosis fac ...... n for the rat small intestine.
@ast
Increase in tumor necrosis fac ...... n for the rat small intestine.
@en
prefLabel
Increase in tumor necrosis fac ...... n for the rat small intestine.
@ast
Increase in tumor necrosis fac ...... n for the rat small intestine.
@en
P2093
P2860
P356
P1476
Increase in tumor necrosis fac ...... n for the rat small intestine.
@en
P2093
Bertrand V
Chaussade S
Chauvelot-Moachon L
Couturier D
Guimbaud R
Mauprivez C
P2860
P304
P356
10.1038/SJ.BJP.0701968
P407
P577
1998-08-01T00:00:00Z