ArticleMolecular biology reports2026
Inhibition of aerobic glycolysis suppresses ferroptosis via activation of the AMPK-FoxO3a pathway in epileptic rats.
Article in Molecular biology reports, 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
backgroundFerroptosis has recently been implicated in seizure-induced neurodegeneration, whereas enhanced aerobic glycolysis during seizures may aggravate oxidative stress and ferroptotic damage. This study investigated whether inhibition of aerobic glycolysis suppresses ferroptosis through activation of the AMP-activated protein kinase (AMPK)-Forkhead box O3a (FoxO3a) signaling pathway in epileptic rats. METHODS AND
resultsA pilocarpine (PILO)-induced epilepsy model was established in male Wistar rats. Animals were treated with the aerobic glycolysis inhibitor 2-deoxy-D-glucose (2-DG), with or without the AMPK inhibitor Compound C. Behavioral evaluation, Morris water maze testing, biochemical assays, immunohistochemistry, quantitative real-time PCR, western blotting, and mitochondrial membrane potential analyses were performed. Epileptic rats exhibited significant upregulation of pyruvate kinase M2 (PKM2), pyruvate dehydrogenase kinase 1 (PDK1), and lactate dehydrogenase A (LDHA), indicating enhanced aerobic glycolysis in the hippocampus. Treatment with 2-DG significantly reduced seizure severity and improved spatial learning and memory. Moreover, inhibition of aerobic glycolysis markedly decreased Fe²⁺ and malondialdehyde (MDA) accumulation, restored glutathione (GSH) and glutathione peroxidase 4 (Gpx4) levels, preserved mitochondrial membrane potential, and enhanced AMPK and FoxO3a activation. These protective effects were substantially reversed by Compound C administration.
conclusionInhibition of aerobic glycolysis attenuates seizure-induced ferroptosis through activation of the AMPK-FoxO3a pathway. These findings establish a mechanistic link between metabolic reprogramming and ferroptosis in epilepsy and suggest that targeting aerobic glycolysis may represent a promising therapeutic strategy for neuroprotection in epilepsy.
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