ArticleCNS neuroscience & therapeutics2019
Baicalin mitigates cognitive impairment and protects neurons from microglia-mediated neuroinflammation via suppressing NLRP3 inflammasomes and TLR4/NF-κB signaling pathway.
Article in CNS neuroscience & therapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 203 papers, 4 of them syntheses that pooled it.
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Who cites it
203 citing papers in PubMed, 4 syntheses or guidelines pooled it, 362 citations in OpenAlex.
- Research progress on microglial pyroptosis and inflammasomes: a comprehensive analysis.Frontiers in aging neuroscience · 2025Pooled it
- Research hotspots and trends on NF-κB in cognitive impairment: a bibliometric analysis.Frontiers in medicine · 2024Pooled it
- Therapeutic benefits of flavonoids against neuroinflammation: a systematic review.Inflammopharmacology · 2022Pooled it
- Hearing loss and dementia: radiologic and biomolecular basis of their shared characteristics. A systematic review.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021Pooled it
- Effect of MALT1 inhibition by MI‑2 on the microglial phenotype switch, inflammatory cytokine secretion, neuronal loss and oxidative stress in Alzheimer's disease.International journal of molecular medicine · 2026Article
- Antiviral Activity of Baicalin Against PRRSV In Vitro and in Infected Piglets.Veterinary sciences · 2026Article
- Regulation of NLRP3 inflammasome signaling in Alzheimer's disease: emerging neuroprotective role of phytochemicals.Inflammopharmacology · 2026Review
- Could the cognitive benefits of amyloid-beta clearance grow in time for Alzheimer's disease?Translational psychiatry · 2026Review
- Olfml3 Regulates Microglial Inflammation and Neuronal Injury in Obstructive Sleep Apnea via Cybb-Mediated TLR4/NF-κB Pathway.CNS neuroscience & therapeutics · 2026Article
- Dexmedetomidine inhibits microglia activation, neuroinflammation, and glycolysis in postoperative cognitive dysfunction by promoting YTHDF2-mediated PKM2 mRNA degradation.Molecular and cellular biochemistry · 2026Article
- Targeting neuroinflammation and PVNMaterials today. Bio · 2026Article
- Nrf2 Modulation by Natural Compounds in Aging, Neurodegeneration, and Neuropathic Pain.Pharmaceutics · 2026Review
- Chinese Herbal Medicine Ultrasonic Atomization Combined with Artificial Tears for Dry Eye Disease in Chinese Populations: A Meta-Analysis of Randomized Controlled Trials.Clinical ophthalmology (Auckland, N.Z.) · 2026Review
- The potential connection between inflammatory bowel disease and Alzheimer's disease: mechanistic insights and therapeutic implications.Frontiers in immunology · 2026Review
- Natural flavonoids in multiple sclerosis: molecular insights and emerging therapeutic strategies.Frontiers in immunology · 2026Review
- Investigating the therapeutic mechanism of Puerarin in vascular dementia: an integrated approach combining network pharmacology and experimental validation.Frontiers in pharmacology · 2026Article
- Article
- Multi-target intervention mechanisms and prospects of the traditional Chinese medicine Scutellaria baicalensis georgi in Alzheimer's disease.Frontiers in pharmacology · 2026Review
- Cell death in uveitis: pyroptosis, ferroptosis, apoptosis, and beyond.Frontiers in immunology · 2026Review
- Flavonoids in Plants and Human Health: From Biosynthesis to Neurodevelopmental and Neurodegenerative Disorders.Molecules (Basel, Switzerland) · 2025Review
143 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsBaicalin (BAI), a flavonoid compound isolated from the root of Scutellaria baicalensis Georgi, has been established to have potent anti-inflammation and neuroprotective properties; however, its effects during Alzheimer's disease (AD) treatment have not been well studied. This study aimed to investigate the effects of BAI pretreatment on cognitive impairment and neuronal protection against microglia-induced neuroinflammation and to explore the mechanisms underlying its anti-inflammation effects.
methodsTo determine whether BAI plays a positive role in ameliorating the memory and cognition deficits in APP (amyloid beta precursor protein)/PS1 (presenilin-1) mice, behavioral experiments were conducted. We assessed the effects of BAI on microglial activation, the production of proinflammatory cytokines, and neuroinflammation-mediated neuron apoptosis in vivo and in vitro using Western blot, RT-PCR, ELISA, immunohistochemistry, and immunofluorescence. Finally, to elucidate the anti-inflammation mechanisms underlying the effects of BAI, the protein expression of NLRP3 inflammasomes and the expression of proteins involved in the TLR4/NF-κB signaling pathway were measured using Western blot and immunofluorescence.
resultsThe results indicated that BAI treatment attenuated spatial memory dysfunction in APP/PS1 mice, as assessed by the passive avoidance test and the Morris water maze test. Additionally, BAI administration effectively decreased the number of activated microglia and proinflammatory cytokines, as well as neuroinflammation-mediated neuron apoptosis, in APP/PS1 mice and LPS (lipopolysaccharides)/Aβ-stimulated BV2 microglial cells. Lastly, the molecular mechanistic study revealed that BAI inhibited microglia-induced neuroinflammation via suppression of the activation of NLRP3 inflammasomes and the TLR4/NF-κB signaling pathway.
conclusionOverall, the results of the present study indicated that BAI is a promising neuroprotective compound for use in the prevention and treatment of microglia-mediated neuroinflammation during AD progression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.