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The non-steroidal anti-inflammatory drug piroxicam blocks ligand binding to the formyl peptide receptor but not the formyl peptide receptor like 1

Artikel i vetenskaplig tidskrift
Författare Anna-Lena Stenfeldt
Jennie Karlsson
Christine Wennerås
Johan Bylund
Huamei Fu
Claes Dahlgren
Publicerad i Biochem Pharmacol
Volym 74
Nummer/häfte 7
Sidor 1050-6
Publiceringsår 2007
Publicerad vid Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning
Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi
Institutionen för biomedicin, avdelningen för infektionssjukdomar
Sidor 1050-6
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

The anti-inflammatory drug piroxicam has been reported to affect the production of reactive oxygen species in phagocytes. This anti-inflammatory effect is thought to be mediated through inhibition of cyclooxygenase (COX), an enzyme important for prostaglandin synthesis. We have compared the effects of piroxicam on superoxide production mediated by two closely related G-protein coupled receptors expressed on neutrophils, the formyl peptide receptor (FPR) and the formyl peptide receptor like 1 (FPRL1). Neutrophils were stimulated with agonists that bind specifically to FPR (the peptide ligand N-formyl-Met-Leu-Phe, fMLF) or FPRL1 (the peptide ligand Trp-Lys-Tyr-Met-Val-L-Met-NH(2), WKYMVM) or both of these receptors (the peptide ligand Trp-Lys-Tyr-Met-Val-D-Met-NH(2), WKYMVm). Piroxicam reduced the neutrophil superoxide production induced by the FPR agonist but had no significant effect on the FPRL1 induced response. Neutrophil intracellular calcium changes induced by the agonist WKYMVm (that triggers both FPR and FPRL1) were only inhibited by piroxicam when the drug was combined with the FPRL1 specific antagonist, Trp-Arg-Trp-Trp-Trp-Trp (WRW(4)), and this was true also for the inhibition of superoxide anion release. Receptor-binding analysis showed that the fluorescently labelled FPR specific ligand N-formyl-Nle-Leu-Phe-Nle-Tyr-Lys (fNLFNYK), was competed for in a dose-dependent manner, by the FPR ligand fMLF and as well as by piroxicam. We show that piroxicam inhibits the neutrophil responses triggered through FPR, but not through FPRL1 and this inhibition is due to a reduced binding of the activating ligand to its cell surface receptor.

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