Genistein Antagonizes Inflammatory Damage Induced by β-amyloid Peptide in Microglia through TLR4 and NF-Κb
Abstract
Objectives Microglia activation and neuroinflammation have been associated with the pathogenesis of neurodegenerative disorders such as Alzheimer's disease (AD). Toll-like receptor 4 (TLR4) and nuclear factor (NF)-κB-mediated signal pathways exert key modulating roles in the inflammatory processes. The aim of the present study was to investigate whether genistein (Gen) has a neuroprotective effect against inflammatory damage induced by β-amyloid peptide25-35 (Aβ25-35) through the TLR4 and NF-κB-mediated signal pathways.Methods BV-2 microglia cells were preincubated with Gen for 2 h and then treated with 25 μM Aβ25-35 for another 24 h. The expression of inflammatory mediators, TLR4 and NF-κB and the activity of NF-κB were measured.Results The results showed that Gen could attenuate the cytotoxicity and inflammatory damage induced by Aβ25-35. Gen also significantly reversed Aβ25-35-induced up-regulation of TLR4 and NF-κB expression and the DNA binding and transcriptional activities of NF-κB.Conclusion These results indicated that Gen could alleviate the inflammation caused by Aβ25-35 treatment, which might be associated with the regulation of the TLR4/NF-κB signal pathway.
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Genistein inhibits NF-kB signaling mediated by TLR4.
“genistein can inhibit the activity of NF-kB signal pathway mediated by Toll-like receptor (TLR4) (Zhou et al., 2014)”
From Exploring the Therapeutic Potential of Phytochemicals in Alzheimer’s Disease: Focus on Polyphenols and Monoterpenes (2022) · cites this paper as Zhou et al., 2014
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- Authors
- Zhou, X., Yuan, L., Zhao, X., Hou, C., Ma, W., Yu, H., & Xiao, R.
- Affiliations
- Capital Medical University (CN)
- Beijing Jishuitan Hospital (CN)
- Corresponding author
- Xiao, Rong
- Venue
- Nutrition
- Publisher
- Elsevier BV
- Published
- 2014-01
- Volume
- 30
- Issue
- 1
- Pages
- 90-95
- ISSN
- 0899-9007 (ISSN-L)
- OpenAlex
- W2129602425
- Cited by
- 89
- References
- 41
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 8 · 2023: 11 · 2022: 11 · 2021: 10 · 2020: 5 · 2019: 7 · 2018: 8 · 2017: 7 · 2016: 4 · 2015: 6 · 2014: 1
- FWCI
- 2.04
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nutrition (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Beijing Municipal Natural Science Foundation (7102015)
- National Natural Science Foundation of China (30972470)
- National High Technology Research and Development Program (863 Program) of China (2010AA023003)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- genistein, amyloid beta 25-35, microglia, neuroinflammation, Alzheimer's disease, TLR4, NF-κB signaling, neuroprotection, BV-2 cells, isoflavones
- MeSH terms
- Alzheimer Disease, Animals, Cell Line, Cell Survival, Inflammation, Peptide Fragments, Signal Transduction, Up-Regulation, Amyloid beta-Peptides, NF-kappa B, Microglia, Neuroprotective Agents, Genistein, Toll-Like Receptor 4, Mice
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