ArticleIranian journal of basic medical sciences2023
Protective effects of baicalin against L-glutamate-induced oxidative damage in HT-22 cells by inhibiting NLRP3 inflammasome activation via Nrf2/HO-1 signaling.
Article in Iranian journal of basic medical sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Quercetin Activates NRF2/SLC7A11/GPX4 Signaling to Restore Mitochondrial Function Inhibit Ferroptosis Thereby Alleviating Doxorubicin-Induced Cardiotoxicity.Biomolecules · 2026Article
- Baicalin: bridging traditional medicine and modern science in food and functional applications.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Baicalin protects neurons from oxidative stress and apoptosis induced by glutamate excitotoxicity in HT-22 cells.Journal of veterinary science · 2025Article
- Neuroprotective Effect of β-Lapachone against Glutamate-Induced Injury in HT22 Cells.Biomolecules & therapeutics · 2025Article
- Neuroprotective effects of baicalin and baicalein on the central nervous system and the underlying mechanisms.Heliyon · 2025Review
- The key players of inflammasomes and pyroptosis in sepsis-induced pathogenesis and organ dysfunction.Frontiers in pharmacology · 2025Review
- Pharmacological mechanisms by which baicalin ameliorates cardiovascular disease.Frontiers in pharmacology · 2024Review
- An interventional study of baicalin on neuronal pentraxin-1, neuronal pentraxin-2, and C-reactive protein in Alzheimer's disease rat model.Translational neuroscience · 2023Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: To explore the ability and underlying molecular mechanisms involved in the protective effects of Baicalin (BA) against L-Glutamate-induced mouse hippocampal neuron cell line HT-22. Materials and Methods: The cell injury model of HT-22 cells was induced by L-glutamate, and cell viability and damage were detected by CCK-8 and LDH assays. Generation of intracellular reactive oxygen species (ROS) was measured by DCFH-DA Results: L-Glutamate exposure induced cell injuries in HT-22 cells, and the concentration of 5 mM L-Glutamate was chosen to be the modeling condition. Co-treatment with BA significantly promoted cell viability and reduced LDH release in a dose-dependent manner. In addition, BA attenuated the L-Glutamate-induced injuries by decreasing the ROS production and MDA concentration, while increasing the SOD activity. Moreover, we also found that BA treatment up-regulated the gene and protein expression of Nrf2 and HO-1, and then inhibited the expression of NLRP3. Conclusion: Our study found that BA could relieve oxidative stress damage of HT-22 cells induced by L-Glutamate, and the mechanism might be related to the activation of Nrf2/HO-1 and inhibition of NLRP3 inflammasome.
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