COX inhibitors downregulate PDE4D expression in a clinical model of inflammatory pain.

R A Dionne, S M Gordon, S M Wahl, X-M Wang, M Hamza

Journal: Clinical pharmacology and therapeutics 2008;84(1):39-42

PMID: 18288087

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Abstract

Tumor necrosis factor-alpha (TNF-alpha) has a central role in inflammation and is modulated by prostaglandin E(2) (PGE(2)) and cyclic adenosine monophosphate (cAMP). Using microarray, quantitative real-time polymerase chain reaction (qRT-PCR), and protein detection techniques, we showed that ketorolac and rofecoxib had no significant effect on TNF-alpha gene expression in oral mucosal biopsies 3 h after surgery. They both, however, downregulated the gene and protein expression of phosphodiesterase type 4 (PDE4D), which might represent a novel mechanism contributing to their analgesic and anti-inflammatory effects.

Address: Pain Research Section, National Institute of Nursing Research, National Institutes of Health, Bethesda, Maryland, USA.

DOI: 10.1038/sj.clpt.6100501

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MeSH Terms: Adolescent, Adult, Cyclic Nucleotide Phosphodiesterases, Type 3, Cyclic Nucleotide Phosphodiesterases, Type 4, Cyclooxygenase Inhibitors, Down-Regulation, Gene Expression Regulation, Enzymologic, Humans, Inflammation, Pain, Phosphodiesterase 3 Inhibitors, Tumor Necrosis Factor-alpha