Ginkgolide B inhibits NLRP3 inflammasome activation and promotes microglial M2 polarization in Aβ1-42-induced microglia cells
Abstract
Nucleotide-binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3) inflammasome-mediated chronic neuroinflammation plays a crucial role in the progression of Alzheimer's disease (AD), which is related to microglial activation. Using quantitative proteomic analysis, we identified 25 up-regulated and 83 down-regulated proteins in amyloid beta (Aβ)1-42-induced BV2 cells. Among the differentiallyexpressedproteins involved in inflammation, the NLRP3 protein level increased dramatically. Ginkgolide B (GB) prevents Aβ-induced neuroinflammation and neurotoxic effects in multiple neurodegenerative disorders. However, its role in NLRP3 inflammasome-mediated neuroinflammation in AD remain unknown. We found that GB treatment ameliorated Aβ 1-42-induced pathological damages and inhibited NLRP3 inflammasome activation. Furthermore, GB enhanced the expression of M2 microglial markers and suppressed the expression of M1 microglial markers. Our findings suggest that GB treatment prevents the pathological processes of AD and suppresses neuroinflammation by inhibiting NLRP3 inflammasome activation and promoting microglial M2 polarization.
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Ginkgolide B exhibits significant anti-Alzheimer's activity.
“Furthermore, in a recent work, a bioactive compound, ginkgolide B (GB), obtained from GB exhibited significant anti-Alzheimer's activity [96].”
From Unlocking the Therapeutic Potential of Medicinal Plants for Alzheimer’s Disease: Preclinical to Clinical Trial Insights (2023) · cites this paper as [96]
Ginkgo biloba protects from clinical manifestations of Alzheimer's disease.
“Thus, GB protects from clinical manifestations of AD [96].”
From Unlocking the Therapeutic Potential of Medicinal Plants for Alzheimer’s Disease: Preclinical to Clinical Trial Insights (2023) · cites this paper as [96]
Ginkgo biloba prevents Aβ-induced neuroinflammation and reduces neuroinflammation by preventing NLRP3 inflammasome activation and stimulating microglial M2 polarization.
“The researchers also suggested that GB prevents Aβ-induced neuroinflammation and reduces neuroinflammation by preventing the activation of the NLRP3 inflammasome in addition to stimulation of microglial M2 polarization.”
From Unlocking the Therapeutic Potential of Medicinal Plants for Alzheimer’s Disease: Preclinical to Clinical Trial Insights (2023) · cites this paper as [96]
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- Authors
- Zhang, Y., Zhao, Y., Zhang, J., Gao, Y., Li, S., Chang, C., Yu, D., & Yang, G.
- Affiliations
- Second Hospital of Hebei Medical University (CN)
- Corresponding author
- Yang, Guofeng
- Venue
- Neuroscience Letters
- Publisher
- Elsevier BV
- Published
- 2021-11
- Volume
- 764
- Pages
- 136206
- ISSN
- 0304-3940 (ISSN-L)
- OpenAlex
- W3196858661
- Cited by
- 36
- References
- 22
- Citations by year
- 2026: 8 · 2025: 8 · 2024: 4 · 2023: 12 · 2022: 4
- FWCI
- 2.00
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Neuroscience Letters (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- ginkgolide B, NLRP3 inflammasome, microglial polarization, M2 microglia, M1 microglia, amyloid-beta 42, Alzheimer's disease, neuroinflammation, BV-2 cells, neuroprotection
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Neuroinflammatory Diseases, Alzheimer Disease, Animals, Disease Models, Animal, Humans, Lactones, Peptide Fragments, Amyloid beta-Peptides, Microglia, Ginkgolides, Mice, Inflammasomes
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