Reports

Clinical Pharmacology & Therapeutics (2008); 84, 1, 39–42 doi:10.1038/sj.clpt.6100501

COX Inhibitors Downregulate PDE4D Expression in a Clinical Model of Inflammatory Pain

X-M Wang1, M Hamza1,2, SM Gordon3, SM Wahl4 and RA Dionne1

  1. 1Pain Research Section, National Institute of Nursing Research, National Institutes of Health, Bethesda, Maryland, USA
  2. 2Department of Pharmacology, Faculty of Medicine, Ain Shams University, Cairo, Egypt
  3. 3Department of Biomedical Sciences, School of Dentistry, University of Maryland, Baltimore, Maryland, USA
  4. 4Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland, USA

Correspondence: RA Dionne, (dionner@mail.nih.gov)

Received 6 September 2007; Accepted 9 December 2007; Published online 20 February 2008.

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Abstract

Tumor necrosis factor-alpha (TNF-alpha) has a central role in inflammation and is modulated by prostaglandin E2 (PGE2) 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.

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