ArticleMetabolic brain disease2022
Ginkgolide B inactivates the NLRP3 inflammasome by promoting autophagic degradation to improve learning and memory impairment in Alzheimer's disease.
Article in Metabolic brain disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- Effect of ginkgo diterpene lactone meglumine on the quality of life in patients with acute ischemic stroke.Health and quality of life outcomes · 2024Trial
- Regulation of NLRP3 inflammasome signaling in Alzheimer's disease: emerging neuroprotective role of phytochemicals.Inflammopharmacology · 2026Review
- Natural products and neurocognitive disorders: Mechanistic insights and research advances (Review).Molecular medicine reports · 2026Review
- Ginkgolide B Alleviates Airway Inflammation in Hyperoxia Lung Injury.Immunity, inflammation and disease · 2026Article
- Ginkgolide B regulates apoptosis, oxidative stress, and mitochondrial dysfunction in MPPNaunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Research Progress in the Molecular Mechanism of NLRP3 Inflammasome in Alzheimer's Disease and Regulation by Natural Plant Products.Molecular neurobiology · 2025Review
- Signs of Alzheimer's Disease: Tied to Aging.International journal of molecular sciences · 2025Review
- NLRP3 inflammasome in Alzheimer's disease: molecular mechanisms and emerging therapies.Frontiers in immunology · 2025Review
- The roles of ubiquitination and deubiquitination of NLRP3 inflammasome in inflammation-related diseases: A review.Biomolecules & biomedicine · 2024Review
- Liposome-Derived Nanosystems for the Treatment of Behavioral and Neurodegenerative Diseases: The Promise of Niosomes, Transfersomes, and Ethosomes for Increased Brain Drug Bioavailability.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Article
- Review
- Autophagy Balances Neuroinflammation in Alzheimer's Disease.Cellular and molecular neurobiology · 2023Review
- NLRP3 Inflammasome's Activation in Acute and Chronic Brain Diseases-An Update on Pathogenetic Mechanisms and Therapeutic Perspectives with Respect to Other Inflammasomes.Biomedicines · 2023Review
- Anti-Neuroinflammatory Potential of Natural Products in the Treatment of Alzheimer's Disease.Molecules (Basel, Switzerland) · 2023Review
- Ginkgolide B Blocks Vascular Remodeling after Vascular Injury via Regulating TgfCardiovascular therapeutics · 2023Article
- A novel strategy for bioactive natural products targeting NLRP3 inflammasome in Alzheimer's disease.Frontiers in pharmacology · 2022Review
- Punicalagin Attenuates LPS-Induced Inflammation and ROS Production in Microglia by Inhibiting the MAPK/NF-κB Signaling Pathway and NLRP3 Inflammasome Activation.Journal of inflammation research · 2022Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The NLR family, pyrin domain containing 3 (NLRP3) inflammasome drives the progression of Alzheimer's disease (AD). Ginkgolide B (GB) is a potential anti-inflammatory compound that controls neuro-inflammation. The aim of this study was to evaluate the effect of GB on the NLRP3 inflammasome in AD. The effect of GB on the conversion between the M1 and M2 microglial phenotype was examined using quantitative real-time PCR and immunostaining. Western blotting assays and ELISA were used to detect changes in neuro-inflammation following GB treatment, including the NLRP3 inflammasome pathway and autophagy. In order to evaluate the cognitive function of male senescence-accelerated mouse prone 8 (SAMP8) mice, behavioral tests, including the Morris water maze and novel object recognition tests, were performed. GB significantly decreased the intracellular pro-inflammatory cytokine levels in lipopolysaccharide-treated BV2 cells and improved cognitive behavior in SAMP8 mice. Moreover, GB deactivated the NLRP3 inflammasome, and this effect was dependent on autophagy. Ubiquitination was associated with GB-induced autophagic NLRP3 degradation. These results were further validated in the hippocampus of SAMP8 mice. Thus, GB exerted a neuroprotective effect on the cognitive function of SAMP8 mice by suppressing the activation of NLRP3 inflammasome via autophagic degradation.
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Registered trials
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