ArticleiScience2026
Propranolol alleviates cerebral infarction through the β2-AR-mediated ERK/NLRP3 pathway.
Article in iScience, 2026. 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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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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9 authors.
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Abstract
Propranolol, a non-selective β-adrenergic receptor (β-AR) blocker, has been shown to reduce brain infarction in mice following ischemic stroke. Transient middle cerebral artery occlusion (tMCAO) mice and BV2 cells subjected to oxygen-glucose deprivation (OGD) were used to assess pathophysiological changes after ischemic stroke through behavioral, biochemical, and pathological analyses. We found that propranolol alleviated brain injury after cerebral infarction, inhibited microglial activation, and reduced the expression of NLRP3 and IL-1β. It also reduced Evans blue (EB) extravasation and enhanced the expression of Occludin, ZO-1, and CD-31. Compared to the tMCAO group, all these pathological changes could be reversed in NLRP3
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