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
- 1Pain Research Section, National Institute of Nursing Research, National Institutes of Health, Bethesda, Maryland, USA
- 2Department of Pharmacology, Faculty of Medicine, Ain Shams University, Cairo, Egypt
- 3Department of Biomedical Sciences, School of Dentistry, University of Maryland, Baltimore, Maryland, USA
- 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.
Abstract
Tumor necrosis factor-
(TNF-) 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- 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.
