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COX Inhibitors Downregulate PDE4D Expression in a Clinical Model of Inflammatory Pain
Author(s) -
Wang XM,
Hamza M,
Gordon SM,
Wahl SM,
Dionne RA
Publication year - 2008
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1038/sj.clpt.6100501
Subject(s) - rofecoxib , clinical pharmacology , analgesic , pharmacology , ketorolac , tumor necrosis factor alpha , downregulation and upregulation , inflammation , gene expression , cyclic adenosine monophosphate , medicine , phosphodiesterase , cyclooxygenase , microarray , chemistry , gene , immunology , enzyme , receptor , biochemistry
Tumor necrosis factor‐α (TNF‐α) 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‐α 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. Clinical Pharmacology & Therapeutics (2008); 84 , 1, 39–42 doi: 10.1038/sj.clpt.6100501