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.
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