Contribution of cyclooxygenase-1-dependent prostacyclin synthesis to bradykinin-induced dermal extravasation
| Autor: | Michael Krybus, Marc Sieradzki, Ehsan Fahimi, Sara Metry, Rolf Nüsing, Gerd Geisslinger, Irina Steiner, Thomas Daldrup, Matthias Lehr, Georg Kojda |
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| Rok vydání: | 2022 |
| Předmět: |
Pharmacology
Male Arachidonate 5-Lipoxygenase Arachidonic Acid Diclofenac Group IV Phospholipases A2 Receptors Prostaglandin Endothelial Cells Ibuprofen General Medicine Bradykinin Epoprostenol Mice Inbred C57BL Mice Prostaglandin-Endoperoxide Synthases Cyclooxygenase 1 Oxygenases Animals Angioedema |
| Zdroj: | Biomedicinepharmacotherapy = Biomedecinepharmacotherapie. 148 |
| ISSN: | 1950-6007 |
| Popis: | Non-allergic angioedema is a potentially life-threatening condition caused by accumulation of bradykinin and subsequent activation of bradykinin type 2 receptors (B2). Since COX activity plays a pivotal role in B2 signaling, the aim of this study was to determine which prostaglandins are the key mediators and which COX, COX-1 or COX-2, is predominantly involved.We used Miles assays to assess the effects of inhibitors of COX, 5-lipoxygenase, epoxyeicosatrienoic acid generation, cytosolic phospholipase AUnspecific COX inhibition by ibuprofen and diclofenac significantly reduced B2-mediated dermal extravasation in C57BL/6 but not COX-1Our findings suggest that COX-1-dependent prostacyclin production is critically involved in dermal extravasation after activation of B2 in small dermal blood vessels. Targeting prostacyclin production and/or signaling appears to be a suitable option for acute treatment of non-allergic angioedema. |
| Databáze: | OpenAIRE |
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