ANTAGONISTS OF PGE2 EP3 RECEPTORS

摘要

PGE2 EP3 receptors affect injury size following cerebral ischemia and induced excitotoxicity. Treatment with selective EP3 antagonists decreases infarct size. In addition, such antagonists can reduce lesions caused by N-methyl-D-aspartic acid-induced acute excitotoxicity. Similarly, genetic deletion of EP3 provides protection against N-methyl-D-aspartic acid-induced toxicity. PGE2, by stimulating EP3 receptors, can contribute to the toxicity associated with cyclooxygenase and that antagonizing this receptor can be used therapeutically to protect against stroke- and excitotoxicity-induced brain damage.