ArticleRedox biology2020
Baicalin combats glutamate excitotoxicity via protecting glutamine synthetase from ROS-induced 20S proteasomal degradation.
Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 109 citations in OpenAlex.
- Trial
- Baicalin and CNS-related diseases: new insights into neuroprotective potentials based on underlying mechanisms.Biochemistry and biophysics reports · 2026Review
- Baicalin Alleviates Chronic Restraint Stress-Induced Depression-like Behavior by Suppressing ROS/HAntioxidants (Basel, Switzerland) · 2026Article
- Baicalin confers neuroprotection in animal models of stroke through its antioxidant and anti-apoptotic effects.Journal of veterinary science · 2025Article
- Role of mitochondrial metabolism in ischemic stroke and natural products intervention.Molecular biology reports · 2025Review
- Review
- Age-Related Meat Flavor Precursors of Naturally Grazed Sunit Sheep: Metabolomics and Transcriptomics Approaches.Foods (Basel, Switzerland) · 2025Article
- The role of astrocyte metabolic reprogramming in ischemic stroke (Review).International journal of molecular medicine · 2025Review
- A Baicalin-Based Functional Polymer in Dynamic Reversible Networks Alleviates Osteoarthritis by Cellular Interactions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Scutellarin Alleviates Neuronal Apoptosis in Ischemic Stroke via Activation of the PI3K/AKT Signaling Pathway.International journal of molecular sciences · 2025Article
- Microglia-Astrocyte Crosstalk in Post-Stroke Neuroinflammation: Mechanisms and Therapeutic Strategies.Current neuropharmacology · 2025Review
- Polyphenolic metabolites inFrontiers in pharmacology · 2025Review
- Functionalized biomimetic nanoparticles are delivered from the nose to the brain for the synergistic targeted treatment of cerebral ischemia/reperfusion injury.Regenerative biomaterials · 2025Article
- Plant-derived polyphenolic compounds for managing schizophrenia: mechanisms and therapeutic potential.Frontiers in pharmacology · 2025Review
- Identification of the Anti-ischemia-reperfusion Injury Effect of Baicalein fromCurrent medicinal chemistry · 2025Article
- Excitotoxic Storms of Ischemic Stroke: A Non-neuronal Perspective.Molecular neurobiology · 2024Review
- Selenomethionine and Allicin Synergistically Mitigate Intestinal Oxidative Injury by Activating the Nrf2 Pathway.Toxics · 2024Article
- Brain-Targeting Emodin Mitigates Ischemic Stroke via Inhibiting AQP4-Mediated Swelling and Neuroinflammation.Translational stroke research · 2024Article
- The potential of baicalin to enhance neuroprotection and mitochondrial function in a human neuronal cell model.Molecular psychiatry · 2024Article
- Lipidomic analysis identifies long-chain acylcarnitine as a target for ischemic stroke.Journal of advanced research · 2024Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMany neuroprotective approaches targeting neurons in animal models fail to provide benefits for the treatment of ischemic stroke in clinic and glial cells have become the targets in some basic studies. Baicalin has neuroprotective effects but the mechanisms related to glial cells are not revealed. This study investigated whether and how baicalin can combat excitotoxicity via protecting the functions of astrocytes in early stage of ischemia/reperfusion (I/R) insult by focusing on glutamine synthetase (GS). EXPERIMENTAL APPROACH: The role of baicalin was explored in primary astrocytes exposed to oxygen-glucose deprivation/reperfusion (OGD/R) and rats subjected to middle cerebral artery occlusion/reperfusion (MCAO/R). KEY
resultsMitochondrial succinate dehydrogenase (SDH) activation led to an excessive production of reactive oxygen species (ROS) via reverse electron transport (RET) under conditions of OGD/R or I/R, which increased the carbonylation and proteasomal degradation of GS in astrocytes. Treatment of baicalin decreased the oxidative stress mediated by SDH and reduced the subsequent loss of GS. This effect increased the glutamate disposal by astrocytes and protected neurons from excitotoxicity in response to I/R insults. CONCLUSIONS AND IMPLICATIONS: Baicalin inactivated SDH to suppress ROS production and protected GS protein stability against oxidative stress, contributing to the improvement of the glutamate disposal and decrease in excitotoxicity. These results suggest that protection of GS stability in astrocytes might be an effective strategy to prevent neuronal injury in acute ischemic stroke.
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