ArticleNeuroprotection (Chichester, England)2026
Post-recanalization administration of rapamycin improves functional outcome and reduces infarct size in a rat model of ischemic stroke.
Article in Neuroprotection (Chichester, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Post-recanalization administration of rapamycin improves functional outcome and reduces infarct size in a rat model of ischemic stroke.Neuroprotection (Chichester, England) · 2026Article
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5 authors.
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Abstract
Aim: Despite advances in endovascular recanalization for ischemic stroke, many patients experience poor outcomes. Adjunct cerebroprotective therapies are needed to improve recovery. The mammalian target of rapamycin complex 1 (mTORC1) inhibitor rapamycin has shown neuroprotective effects in preclinical stroke models. However, most studies administered rapamycin prior to or during stroke onset, limiting translational relevance. The aim of this study was to determine whether rapamycin administered immediately after recanalization improves infarct size and functional outcome, and whether these effects are associated with changes in cerebral blood flow (CBF) or blood-brain barrier (BBB) integrity. Methods: Male Wistar Han rats were subjected to transient middle cerebral artery occlusion (tMCAO) for 90 min. Animals were randomized using the sealed envelope method to receive intravenous rapamycin (250 μg/kg, Results: Rapamycin significantly reduced infarct volume compared with vehicle (44.77 ± 30.93 mm³ vs. 113.44 ± 60.19 mm³, Discussion: Rapamycin administered after recanalization improves functional outcomes and reduces infarct size, without altering sustained perfusion or BBB permeability. These findings highlight a perfusion-independent, time-sensitive cerebroprotective mechanism and support rapamycin's development as an adjunctive therapy in ischemic stroke.
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