ArticleJournal of inflammation research2025
Lactate Ameliorates Kainic Acid-Induced Neuroinflammation and Cognitive Impairment via the Chemokine Signaling Pathway in Mice.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- Lactate and cognition: a dual modulator.Frontiers in molecular neuroscience · 2026Review
- Beyond Fuel: Exercise-Induced Lactate as a Metabolic-Epigenetic Regulator in Central Nervous System Health and Disease.Biomolecules · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Lactate, previously considered a metabolic waste product, has been shown to have neuroprotective potential. This study aims to investigate the impact of lactate intervention and its underlying mechanisms on epilepsy. Methods: HT22 cells were stimulated with glutamate to construct an excitotoxicity cell model. An acute epilepsy model was established in mice by kainic acid induction. The neuronal damage, microglial activation, inflammatory responses, and functional changes were determined by TUNEL assays, immunohistochemistry, quantitative real-time polymerase chain reaction and behavioral tests. The differentially gene expression and functional enrichment were analyzed with RNA sequencing. Results: The in vitro lactate intervention reduced the number of apoptotic cells, the release of inflammatory factors, and the expression of vesicular glutamate transporter 1. In mice with acute epilepsy, lactate treatment mitigated neuronal damage, microglial activation, and inflammatory responses in the hippocampus and ameliorated anxiety-like behavior and cognitive impairment. Conclusion: Lactate exerts therapeutic effects on epilepsy through the chemokine signaling pathway. The neuroinflammation is an important contributor to cognitive impairment. Targeting inflammatory pathways is a promising strategy for improving the prognosis of epilepsy.
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Registered trials
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