Suppressing the Inflammatory Prostaglandin Signaling after Thrombotic Stroke Ameliorates Ischemic Brain Injury and Facilitates Poststroke Recovery.

ABSTRACT: Acute cerebral ischemia is a leading cause of death and disability, particularly among old adults. The narrow therapeutic window and risk of hemorrhagic transformation largely limit patient eligibility for the current treatment. The neuroinflammatory signaling pathway involving the prostaglandin E2 (PGE₂) receptor subtype EP2 has now been clarified to contribute to the secondary neurotoxicity following ischemic stroke. We previously demonstrated the feasibility of pharmacologically targeting EP2 for ischemic stroke using an EP2 antagonist in a mouse model of transient middle cerebral artery occlusion. Herein, we evaluated the effects of a second-generation EP2 antagonist with improved potency and selectivity in a mouse model of thrombotic stroke, the most common type of stroke.

SUBMITTER: Jin Z 

PROVIDER: S-EPMC11650728 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature