ArticleFrontiers in pharmacology2026
Crude Astragalus polysaccharides ameliorate cognitive impairment by preserving blood-brain barrier integrity and suppressing GSDMD-mediated pyroptosis in jellyfish-envenomed mice.
Article in Frontiers in pharmacology, 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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Abstract
Introduction: Jellyfish envenomation is an escalating global health threat that can induce severe neurotoxic consequences, but effective therapeutic strategies remain limited. This study investigated whether crude astragalus polysaccharides (APS) protect against jellyfish venom-induced cognitive impairment and explored the underlying mechanisms involving blood-brain barrier (BBB) integrity and pyroptosis. Methods: A murine jellyfish envenomation model was established by intravenous venom injection. Mice were treated with APS, edaravone, or the Caspase-1-specific inhibitor VX-765. Behavioral performance was evaluated using the open field test and Morris water maze. Histopathological injury, cerebral edema, BBB permeability, tight junction protein expression, matrix metalloproteinase-9 (MMP9) expression, inflammasome/pyroptosis-related markers, and inflammatory cytokines were assessed using H&E staining, wet/dry weight measurement, Evans blue extravasation, western blotting, RT-qPCR, and ELISA. Results: APS ameliorated venom-induced anxiety-like behaviors, locomotor deficits, and spatial memory impairment. Histopathologically, APS preserved hippocampal neuronal integrity and attenuated cerebral edema and hemorrhage. APS also reduced BBB disruption by suppressing MMP9 upregulation and restoring tight junction proteins, including ZO-1, Occludin, and Claudin-5. In addition, APS decreased JNK1 expression and inhibited activation of the NLRP3/Caspase-1/GSDMD pyroptotic pathway, as shown by reduced NLRP3 expression, Caspase-1 cleavage, GSDMD-N formation, and inflammatory cytokine release. VX-765 recapitulated the inhibitory effects of APS on pyroptotic markers and cytokines, including IL-1β, IL-18, and TNF-α. Co-administration of APS and VX-765 produced no additive benefit. Discussion: These findings indicate that APS protects against jellyfish venom-induced neurotoxicity mainly by preserving BBB integrity and suppressing canonical Caspase-1-dependent GSDMD-mediated pyroptosis. APS may therefore represent a potential therapeutic candidate for marine envenomation-associated neurological injury.
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