ArticleExperimental and therapeutic medicine2025
Selective Epac2 antagonist attenuates cerebral infarction induced by secondary brain injury in rats.
Article in Experimental and therapeutic medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The impact of 1,3,5-trimethyl-2-[(4-methylphenyl)sulfonyl]-benzene (ESI-05), a specific antagonist of exchange protein directly activated by cyclic adenosine monophosphate 2 (Epac2), in mitigating secondary brain injury following cerebral hemorrhage and trauma has been established. However, to the best of our knowledge, the precise influence of ESI-05 on apoptosis and cell death after cerebral infarction remains uncertain. The present study investigated the involvement of ESI-05 in apoptosis and cell death using a rodent model of cerebral infarction induced by permanent middle cerebral artery (MCA) occlusion. Before permanent MCA occlusion, ESI-05 was administered intraperitoneally at 8 mg/kg. Stroke volume, brain edema, and the levels of Epac2, phospho-p38 and cleaved caspase 3 were evaluated. Apoptosis was detected by TUNEL staining. ESI-05 administration reduced the infarct volume and water content, and reduced the levels of Epac2, phospho-p38 and cleaved caspase 3 in the ischemic penumbra. Immunohistochemical staining confirmed that ESI-05 attenuated apoptosis around the ischemic core. ESI-05 administration reduced apoptosis and cell death around the ischemic core, resulting in amelioration of cerebral edema.
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