Resveratrol Mitigates Lipopolysaccharide- and Aβ-Mediated Microglial Inflammation by Inhibiting the TLR4/NF-Κb/STAT Signaling cascade
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Activation of microglia, the resident macrophages of the brain, around the amyloid plaques is a key hallmark of Alzheimer's disease (AD). Recent evidence in mouse models indicates that microglia are required for the neurodegenerative process of AD. Amyloid-β (Aβ) peptides, the core components of the amyloid plaques, can trigger microglial activation by interacting with several Toll-like receptors (TLRs), including TLR4. In this study, we show that resveratrol, a natural polyphenol associated with anti-inflammatory effects and currently in clinical trials for AD, prevented the activation of murine RAW 264.7 macrophages and microglial BV-2 cells treated with the TLR4 ligand, lipopolysaccharide (LPS). Resveratrol preferentially inhibited nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) activation upon LPS stimulation by interfering with IKK and IκB phosphorylation, an effect that potently reduced the transcriptional stimulation of several NF-κB target genes, including tumor necrosis factor-α and interleukin-6. Consequently, downstream phosphorylation of signal transducer and activator of transcription (STAT)1 and STAT3 upon LPS stimulation was also inhibited by resveratrol. We found that resveratrol acted upstream in the activation cascade by interfering with TLR4 oligomerization upon receptor stimulation. Resveratrol treatment also prevented the pro-inflammatory effect of fibrillar Aβ on macrophages by potently inhibiting the effect of Aβ on IκB phosphorylation, activation of STAT1 and STAT3, and on tumor necrosis factor-α and interleukin-6 secretion. Importantly, orally administered resveratrol in a mouse model of cerebral amyloid deposition lowered microglial activation associated with cortical amyloid plaque formation. Together this work provides strong evidence that resveratrol has in vitro and in vivo anti-inflammatory effects against Aβ-triggered microglial activation. Further studies in cell culture systems showed that resveratrol acted via a mechanism involving the TLR4/NF-κB/STAT signaling cascade.
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Resveratrol inhibits microglial activation in APP/PS1 mice.
“to inhibit microglial activation in APP/PS1 mice (Capiralla et al., 2012)”
From Exploring the Therapeutic Potential of Phytochemicals in Alzheimer’s Disease: Focus on Polyphenols and Monoterpenes (2022) · cites this paper as Capiralla et al., 2012
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- Authors
- Capiralla, H., Vingtdeux, V., Zhao, H., Sankowski, R., Al‐Abed, Y., Davies, P., & Marambaud, P.
- Affiliations
- Feinstein Institute for Medical Research (US)
- Albert Einstein College of Medicine (US)
- Corresponding author
- Marambaud, Philippe
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2011-12-16
- Volume
- 120
- Issue
- 3
- Pages
- 461-472
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- PMC
- PMC3253186
- OpenAlex
- W1589993557
- Cited by
- 426
- References
- 79
- Citations by year
- 2026: 11 · 2025: 32 · 2024: 29 · 2023: 26 · 2022: 35 · 2021: 37 · 2020: 43 · 2019: 40 · 2018: 37 · 2017: 34 · 2016: 21 · 2015: 26 · 2014: 26 · 2013: 21 · 2012: 8
- FWCI
- 9.71
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (R37AG022102, R01AG022102)
- National Center for Complementary and Integrative Health (P01AT004511)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- resveratrol, microglial activation, Alzheimer's disease, amyloid-beta, lipopolysaccharide, TLR4, NF-κB signaling, STAT1, STAT3, IκB phosphorylation, IκB kinase, neuroinflammation, TNF-α, interleukin-6, amyloid plaques, anti-inflammatory polyphenols
- MeSH terms
- NF-KappaB Inhibitor alpha, Resveratrol, Alzheimer Disease, Animals, Anti-Inflammatory Agents, Non-Steroidal, Cell Line, Transformed, Disease Models, Animal, Drug Interactions, Humans, Lipopolysaccharides, Male, Mice, Transgenic, Stilbenes, Time Factors, Tumor Necrosis Factor-alpha, Signal Transduction, Cytokines, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Microglia, Statistics, Nonparametric, Inflammation Mediators, I-kappa B Proteins, Toll-Like Receptors, Mice, Presenilin-1
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