The Anti-rheumatic Gold Salt Aurothiomalate Suppresses Interleukin-1β-induced Hyaluronan Accumulation by Blocking HAS1 Transcription and by Acting as a COX-2 Transcriptional Repressor

Stuhlmeier, Karl M.

doi:10.1074/jbc.m605011200

Cited by 19 publications

(13 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Activation of the NF-κB results in the up-regulation of a group of responsive genes that contribute to inflammation including iNOS and COX-2 [35,36]. Previous studies showed that NF-κB is an important regulator in the induction of iNOS and COX-2 in chondrocytes and synovial cells [37,38]. In the current study, IL-1β induced the degradation of IκB-α in chondrocytes and this degradation was blocked by morin.…”

Section: Discussionmentioning

confidence: 45%

Morin inhibits interleukin-1β-induced nitric oxide and prostaglandin E2 production in human chondrocytes

Chen

Wang

Tang

et al. 2012

International Immunopharmacology

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 45%

Morin inhibits interleukin-1β-induced nitric oxide and prostaglandin E2 production in human chondrocytes

Chen

Wang

Tang

et al. 2012

International Immunopharmacology

View full text Add to dashboard Cite

“…They observed that the molecular size of the biopolymer fragments produced by RA fibroblasts were shifted towards normal HA molar-mass values. Stuhlmeier [17] found out that aurothiomalate decreased HA release from fibroblasts by the drug interference with HA synthase 1.…”

mentioning

confidence: 99%

Aurothiomalate as Preventive and Chain‐Breaking Antioxidant in Radical Degradation of High‐Molar‐Mass Hyaluronan

Valachová

Vargová

Rapta

et al. 2011

Chemistry & Biodiversity

View full text Add to dashboard Cite

The potential anti- or pro-oxidative effects of a disease-modifying antirheumatic drug, aurothiomalate, to protect high-molar-mass hyaluronan against radical degradation were investigated along with L-glutathione - tested in similar functions. Hyaluronan degradation was induced by the oxidative system Cu(II) plus ascorbate known as the Weissberger's oxidative system. The time- and dose-dependent changes of the dynamic viscosity of the hyaluronan solutions were studied by the method of rotational viscometry. Additionally, the antioxidative activity of aurothiomalate expressed as a radical-scavenging capacity based on a decolorization 2,2'-azinobis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) assay was inspected. At the higher concentrations tested, L-glutathione showed excellent scavenging of (.) OH and peroxyl-type radicals, however, at the lowest concentration applied, its pro-oxidative effect was revealed. The effects of aurothiomalate on hyaluronan degradation were similar to that of L-glutathione, however, at the lowest concentration tested, no significant pro-oxidant effect was observed.

show abstract

“…Once activated, NF-κB unit p50 dissociates from its inhibitory protein IκBα and translocates from the cytoplasm to the nucleus where it may trigger the transcription of specific target genes such as iNOS and COX-2 [15]. Previous studies showed that NF-κB is an important regulator in the induction of iNOS and COX-2 in chondrocytes and synovial cells [33]. Therefore, the inhibition of NF-κB activation, through active Se metabolites and selenoproteins, is a possible approach to reduce cytokines and other inflammatory molecules.…”

Section: Discussionmentioning

confidence: 98%

SeMet Mediates Anti-inflammation in LPS-Induced U937 Cells Targeting NF-κB Signaling Pathway

et al. 2014

View full text Add to dashboard Cite

In previous studies, selenium (Se) was reported to play critical roles in anti-inflammatory activities. Nevertheless, limited information could be obtained during inflammation about selenomethionine (SeMet) in U937 human macrophage cells. The purpose of this study was to investigate the effects of SeMet on the inflammatory responses to lipopolysaccharide (LPS)-induced U937 macrophage cells and the signaling pathways targeted. U937 cells were pretreated with SeMet (1 μM) and subsequently induced with LPS (1 μg/ml) for 24 h. In the cell counting kit-8 assay (CCK-8), SeMet significantly inhibits the proliferation of U937 cells. SeMet also inhibited the production of nitric oxide (NO) and prostaglandin E2 (PGE2) stimulated by LPS. In the Western blot assay and real-time polymerase chain reaction (RT-PCR), SeMet significantly reduced protein expression and production of inducible NO synthase (iNOS), tumor necrosis factor-alpha (TNF-α), and COX-2 in U937 cells. Furthermore, SeMet markedly suppressed the LPS-mediated activation of nuclear factor-kappa B (NF-κB) by blocking the degradation of inhibitor-κB proteins (IκBα) and lessening the translocations of P50 subunit content of NF-κB in the nucleus. These findings suggested the anti-inflammatory activity of SeMet in U937 cells; indicating that SeMet might be a potential treatment for inflammation therapy.

show abstract

The Anti-rheumatic Gold Salt Aurothiomalate Suppresses Interleukin-1β-induced Hyaluronan Accumulation by Blocking HAS1 Transcription and by Acting as a COX-2 Transcriptional Repressor

Cited by 19 publications

References 47 publications

Morin inhibits interleukin-1β-induced nitric oxide and prostaglandin E2 production in human chondrocytes

Morin inhibits interleukin-1β-induced nitric oxide and prostaglandin E2 production in human chondrocytes

Aurothiomalate as Preventive and Chain‐Breaking Antioxidant in Radical Degradation of High‐Molar‐Mass Hyaluronan

SeMet Mediates Anti-inflammation in LPS-Induced U937 Cells Targeting NF-κB Signaling Pathway

Contact Info

Product

Resources

About