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 EP2
receptors and intracerebral hemorrhage were searched
in PubMed, Medline, and Ebase.
Results: Previous studies showed that EP2
receptor mediated double effects in ICH via
different signaling pathway. EP2 receptor could induce neuroprotection, spatial learning, and neuroplasticity
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.