ArticleInternational journal of nanomedicine2026
Neuroprotective Delivery of Dexmedetomidine Liposomes Mitigates Cerebral Energy Crisis by Modulating Calcium-Driven Aerobic Glycolysis in Cerebral Ischemia-Reperfusion Injury.
Article in International journal of nanomedicine, 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: Cerebral ischemia-reperfusion injury (CIRI) involves complex pathogenesis with limited therapeutic options. This study investigated whether dexmedetomidine liposomes (Dex-lip) exert neuroprotective effects by modulating astrocytic aerobic glycolysis via calcium signaling. Methods: In vivo CIRI model mice received Dex-lip, with or without the aerobic glycolysis inhibitor 2-deoxy-D-glucose (2-DG). Neurological function, cortical calcium levels, aerobic glycolysis-related protein expression, lactate production, and hippocampal neuronal damage were assessed. In vitro, astrocytes were treated with the calcium channel blocker nifedipine to evaluate intracellular calcium, lactate levels, and glycolysis-related gene expression. Results: Dex-lip treatment reduced cortical calcium overload, upregulated aerobic glycolysis key proteins, increased lactate production, and attenuated hippocampal neuronal injury. These neuroprotective effects were abolished by 2-DG. In vitro, nifedipine lowered astrocytic calcium concentration, which paradoxically increased lactate production, elevated ECAR, and upregulated HK1, HK2, and PFK1 mRNA expression, confirming that calcium reduction promotes aerobic glycolysis. Conclusion: Dex-lip ameliorates CIRI by reducing astrocytic calcium overload, enhancing aerobic glycolysis and lactate supply to neurons, thereby preventing apoptosis. This study provides a mechanistic basis and therapeutic strategy for CIRI.
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