ArticleJournal of veterinary science2025
Baicalin protects neurons from oxidative stress and apoptosis induced by glutamate excitotoxicity in HT-22 cells.
Article in Journal of veterinary science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Baicalin alleviates Trueperella pyogenes-induced endometritis with associated changes in gut microbiota composition.BMC veterinary research · 2026Article
- Six New Phenolic Compounds in Ethyl Acetate Extract of Tall Gastrodia Tuber (Tianma) with Four Compounds Screened Preliminarily for Cytoprotective Effects Against Excitotoxicity.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Gas6 restores microglial efferocytosis and limits neuroinflammation in neonatal hypoxic-ischemic encephalopathy by activating MerTK and the PI3K-Rac1 pathway.Cell communication and signaling : CCS · 2026Article
- Baicalin Alleviates Chronic Restraint Stress-Induced Depression-like Behavior by Suppressing ROS/HAntioxidants (Basel, Switzerland) · 2026Article
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Authors and funding
2 authors.
Funding
Abstract
importanceBaicalin is a flavonoid compound with various functions, including neuroprotective effects. Glutamate is an essential excitatory neurotransmitter involved in synaptic transmission, but it can also induce neuronal damage through excitotoxicity.
objectiveTo analyze the anti-oxidant and anti-apoptotic effects of baicalin on glutamate-exposed neuronal cells.
methodsMouse neuronal hippocampal HT-22 cells were cultured and treated with glutamate (5 mM) and/or baicalin (10, 30, 50 µM). Baicalin was administered 1 h before glutamate treatment, and cells were collected 24 h following glutamate exposure. Reactive oxygen species (ROS) and lipid peroxidation (LPO) analyses were performed to determine the oxidative stress. Western blot and immunocytochemical staining were performed to investigate the expressions of bcl-2, bax, and caspase-3.
resultsGlutamate induced severe neuronal damage, including cell morphological condensation, which was attenuated by baicalin treatment. Baicalin treatment ameliorated the decrease in cell viability due to glutamate toxicity. Baicalin mitigated glutamate-induced increase of ROS and LPO in a dose-dependent manner. Glutamate exposure induced the downregulation of bcl-2 and the upregulation of bax, thereby reducing the bcl-2 to bax ratio, while administration of baicalin prevented these changes. Baicalin treatment ameliorated the glutamate toxicity-induced increase in caspase-3. CONCLUSIONS AND RELEVANCE: Baicalin exerts antioxidant and anti-apoptotic functions against glutamate toxicity in neurons by preventing oxidative stress and inhibiting the apoptotic pathway.
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