前列腺素E2 EP2受体在脑内出血中的双重作用

Title:The Double Roles of the Prostaglandin E₂ EP2 Receptor in Intracerebral Hemorrhage

Volume: 18 Issue: 12

关键词: 脑内出血，前列腺素E2，EP2受体，ICH引起的脑损伤。

摘要: Background: Intracerebral hemorrhage (ICH), a subtype of stroke, brings high morbidity and mortality to human beings. Multiple studies indicated that neuroinflammation, excitotoxicity, oxidative stress, cytotoxicity resulted from the degradation products of blood clot play vital roles in ICH-induced secondary brain injury, which contributes to deterioration of neurological outcome. Prostaglandin E2 (PGE2), a type of prostanoids commonly up-regulated in these progresses, is proved to modulate numerous cellular and molecular processes by activating EP₂ receptor after ICH.

Objective: This review aim to discuss the PGE2 biosynthesis, downstream signaling pathway of EP₂ receptor and the roles of EP₂ receptor in ICH-induced brain damage, targeting to provide a potential effective therapeutic strategy.

Methods: A large number of literatures on EP₂receptors and intracerebral hemorrhage were searched in PubMed, Medline, and Ebase.

Results: Previous studies showed that EP₂ receptor mediated double effects in ICH via activation of different signaling pathway. EP2 receptor could induce neuroprotection, spatial learning, and neuroplasticity via cAMP-PKA signaling pathway, while strengthen inflammation mainly through the cAMP-Epac pathway. In addition, the concentration level of cAMP might be the key factor that decides which downstream signaling pathway would be activated.

Conclusion: In different phase of cerebral hemorrhage, EP2 receptor plays diverse effects in brain damage through different downstream signaling pathways.

Cite this article as:

The Double Roles of the Prostaglandin E₂ EP2 Receptor in Intracerebral Hemorrhage, Current Drug Targets 2017; 18 (12) . https://dx.doi.org/10.2174/1389450117666151209122826

DOI https://dx.doi.org/10.2174/1389450117666151209122826	Print ISSN 1389-4501
Publisher Name Bentham Science Publisher	Online ISSN 1873-5592