Literature DB >> 17275922

Stimulation of prostaglandin E2-EP3 receptors exacerbates stroke and excitotoxic injury.

Muzamil Ahmad1, Abdullah Shafique Ahmad, Hean Zhuang, Takayuki Maruyama, Shuh Narumiya, Sylvain Doré.   

Abstract

The effect of PGE(2) EP3 receptors on injury size was investigated following cerebral ischemia and induced excitotoxicity in mice. Treatment with the selective EP3 agonist ONO-AE-248 significantly and dose-dependently increased infarct size in the middle cerebral artery occlusion model. In a separate experiment, pretreatment with ONO-AE-248 exacerbated the lesion caused by N-methyl-d-aspartic acid-induced acute excitotoxicity. Conversely, genetic deletion of EP3 provided protection against N-methyl-d-aspartic acid-induced toxicity. The results suggest that PGE(2), by stimulating EP3 receptors, can contribute to the toxicity associated with cyclooxygenase and that antagonizing this receptor could be used therapeutically to protect against stroke- and excitotoxicity-induced brain damage.

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Year:  2007        PMID： 17275922      PMCID： PMC1914218          DOI： 10.1016/j.jneuroim.2006.12.012

Source DB:  PubMed          Journal:  J Neuroimmunol        ISSN： 0165-5728            Impact factor:   3.478


  49 in total

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9.  The PGE2 EP2 receptor and its selective activation are beneficial against ischemic stroke.

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Review 10.  Pathophysiological Roles of Cyclooxygenases and Prostaglandins in the Central Nervous System.

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