GPCR antagonists as an alternative to COX-2 inhibitors: a case for the PGE2 EP1 receptor.
A recent article supports the concept that prostaglandin (PG)E(2) EP(1)-receptor antagonists reduce stroke severity and cell damage; could these agents become a substitute for cyclooxygenase (COX)-2 inhibitors? The total activity of COXs--rate-limiting enzymes of PGE(2) synthesis--increases following acute neurological insult. Drugs that offer the beneficial anti-inflammatory and neuroprotective effects of PGs but that limit the negative effects of COX-2 inhibition could provide the next generation of treatment for acute neuronal damage.
Doré
Sylvain
S
Departments of Anesthesiology and Critical Care Medicine, and Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. sdore@jhmi.edu
D052246:Cyclooxygenase 2 Inhibitors / Q000627:therapeutic use*; D006801:Humans; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D018078:Receptors, Prostaglandin E / Q000037:antagonists & inhibitors* / Q000502:physiology; D058306:Receptors, Prostaglandin E, EP1 Subtype; D020521:Stroke / Q000188:drug therapy
D052246:Cyclooxygenase 2 Inhibitors; D018696:Neuroprotective Agents; C545635:PTGER1 protein, human; D018078:Receptors, Prostaglandin E; D058306:Receptors, Prostaglandin E, EP1 Subtype