Sulindac metabolism and synergy with tumor necrosis factor-alpha in a drug-inflammation interaction model of idiosyncratic liver injury.
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Trovafloxacin enhances lipopolysaccharide-stimulated production of tumor necrosis factor-α by macrophages: role of the DNA damage response.Oxidative stress is important in the pathogenesis of liver injury induced by sulindac and lipopolysaccharide cotreatmentComparison of TNFα to lipopolysaccharide as an inflammagen to characterize the idiosyncratic hepatotoxicity potential of drugs: Trovafloxacin as an example.Neutrophil-cytokine interactions in a rat model of sulindac-induced idiosyncratic liver injuryAmiodarone exposure during modest inflammation induces idiosyncrasy-like liver injury in rats: role of tumor necrosis factor-alpha.Trovafloxacin-induced replication stress sensitizes HepG2 cells to tumor necrosis factor-alpha-induced cytotoxicity mediated by extracellular signal-regulated kinase and ataxia telangiectasia and Rad3-relatedThymoquinone and curcumin attenuate gentamicin-induced renal oxidative stress, inflammation and apoptosis in rats.Cytotoxic Synergy Between Cytokines and NSAIDs Associated With Idiosyncratic Hepatotoxicity Is Driven by Mitogen-Activated Protein KinasesCalcium Contributes to the Cytotoxic Interaction Between Diclofenac and CytokinesRecent advances in 2D and 3D in vitro systems using primary hepatocytes, alternative hepatocyte sources and non-parenchymal liver cells and their use in investigating mechanisms of hepatotoxicity, cell signaling and ADME.Chlorpromazine-induced hepatotoxicity during inflammation is mediated by TIRAP-dependent signaling pathway in miceTrovafloxacin potentiation of lipopolysaccharide-induced tumor necrosis factor release from RAW 264.7 cells requires extracellular signal-regulated kinase and c-Jun N-Terminal Kinase.Biomarkers for drug-induced liver injury.Animal models of idiosyncratic drug-induced liver injury--current status.Central role of mitochondria in drug-induced liver injury.Role of immune reactions in drug-induced liver injury (DILI).Current challenges and controversies in drug-induced liver injury.Non-steroidal anti-inflammatory drugs: What is the actual risk of liver damage?Synergistic Cytotoxicity from Drugs and Cytokines In Vitro as an Approach to Classify Drugs According to Their Potential to Cause Idiosyncratic Hepatotoxicity: A Proof-of-Concept Study.
P2860
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P2860
Sulindac metabolism and synergy with tumor necrosis factor-alpha in a drug-inflammation interaction model of idiosyncratic liver injury.
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article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on 28 July 2009
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
Sulindac metabolism and synerg ...... of idiosyncratic liver injury.
@en
Sulindac metabolism and synerg ...... of idiosyncratic liver injury.
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type
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Sulindac metabolism and synerg ...... of idiosyncratic liver injury.
@en
Sulindac metabolism and synerg ...... of idiosyncratic liver injury.
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prefLabel
Sulindac metabolism and synerg ...... of idiosyncratic liver injury.
@en
Sulindac metabolism and synerg ...... of idiosyncratic liver injury.
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P2093
P2860
P356
P1476
Sulindac metabolism and synerg ...... of idiosyncratic liver injury
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P2093
Erica M Sparkenbaugh
Husam S Younis
Kevin M Beggs
Patricia E Ganey
Robert A Roth
P2860
P304
P356
10.1124/JPET.109.156331
P407
P577
2009-07-28T00:00:00Z