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Mechanisms of pparγ activation by non-steroidal anti-inflammatory drugs and GQ16.


ABSTRACT: This study was undertaken to assess the similarities (or differences) between the well-established PPARγ agonist Rosiglitazone and Non-steroidal anti-inflammatory drugs (NSAIDs) diclofenac, indomethacin and ibuprofen, as well as the partial agonist GQ16 at the transcriptome level. Assessment of NSAID and GQ16 activities in PPARγ-dependent 3T3-L1 cells reveals that NSAIDs and GQ16 display similar effects toward PPARγ-dependent target genes in a manner similar to that of Rosiglitazone. Overall design: Murine 3T3-L1 preadipocytes were differentiated into adipocytes (7 days), then treated with DMSO (control), 100nM rosiglitazone, 25μM sodium diclofenac, 10μM indomethacin, 75μM ibuprofen, or 10μM GQ16 for 24 hours, after which total RNA was isolated.

INSTRUMENT(S): Illumina MouseWG-6 v2.0 expression beadchip

ORGANISM(S): Mus Musculus

SUBMITTER: Paul Webb  

PROVIDER: GSE64075 | GEO | 2015-06-01

SECONDARY ACCESSION(S): PRJNA270064

REPOSITORIES: GEO

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Publications

Mechanisms of peroxisome proliferator activated receptor γ regulation by non-steroidal anti-inflammatory drugs.

Puhl Ana C AC   Milton Flora A FA   Cvoro Aleksandra A   Sieglaff Douglas H DH   Campos Jéssica C L JC   Bernardes Amanda A   Filgueira Carly S CS   Lindemann Jan Lammel JL   Deng Tuo T   Neves Francisco A R FA   Polikarpov Igor I   Webb Paul P  

Nuclear receptor signaling 20151005


Non-steroidal anti-inflammatory drugs (NSAIDs) display anti-inflammatory, antipyretic and analgesic properties by inhibiting cyclooxygenases and blocking prostaglandin production. Previous studies, however, suggested that some NSAIDs also modulate peroxisome proliferator activated receptors (PPARs), raising the possibility that such off target effects contribute to the spectrum of clinically relevant NSAID actions. In this study, we set out to understand how peroxisome proliferator activated rec  ...[more]

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