Cited by 199Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsNeurological Disease Mechanisms and Treatments

Anti-neuroinflammatory Effect of Short-Chain Fatty Acid Acetate against Alzheimer’s Disease via Upregulating GPR41 and Inhibiting ERK/JNK/NF-κB

Liu, Jiaming, Li, Haijun, Gong, Tianyu, Chen, Wenyang, Mao, Shiyin, Kong, Yu, Yu, Jiaheng, Sun, Jing·2020·Journal of Agricultural and Food Chemistry

Abstract

Alzheimer's disease (AD) is a high-incidence neurodegenerative disease in the elderly. Acetate (Ace) is a short-chain fatty acid (SCFA) with neuroprotective activity. The purpose of this study was to investigate the effects and its possible mechanisms of SCFA Ace on AD. A male APP/PS1 transgenic mouse was given intragastric administration Ace for 4 weeks. Cognitive function and microglia activation in mice were assessed. Furthermore, Ace pretreated amyloid-β (Aβ)-induced BV2 microglia, and the levels of CD11b, COX-2, and G-protein-coupled receptor 41 (GPR41) and phosphorylation of ERK, JNK, and NF-κB p65 were determined. Our results revealed that Ace significantly attenuated the cognitive impairment and decreased the CD11b level in the APP/PS1 mice. Moreover, Ace inhibited the phosphorylation of NF-κB p65, ERK, and JNK and decreased the levels of COX-2 and interleukin 1β in the Aβ-stimulated BV2 microglia. Finally, Ace increased the GPR41 level in the Aβ-stimulated BV2 cells. The finding indicated that Ace exerted antineuroinflammatory effects via the upregulation of GPR41 and suppression of the ERK/JNK/NF-κB pathway, which might provide an alternative therapy strategy of AD.

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Crossref · 10.1021/acs.jafc.0c02807

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  • Acetate exerts anti-inflammatory effects in Aβ-induced BV-2 microglial cells by upregulating GPR41 and inhibiting the ERK/JNK/NF-κB signaling pathway.

    “In addition, an in vitro study has demonstrated that acetate exerts anti-inflammatory effects in Aβ-induced BV-2 microglial cells by upregulating the levels of GPR41 and inhibiting the ERK/JNK/NF-κB signaling pathway.285”

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Authors
Liu, J., Li, H., Gong, T., Chen, W., Mao, S., Kong, Y., Yu, J., & Sun, J.
Affiliations
  • Wenzhou Medical University (CN)
  • Taizhou Second People's Hospital (CN)
Corresponding author
Sun, Jing
Venue
Journal of Agricultural and Food Chemistry
Published
2020-06-25
Volume
68
Issue
27
Pages
7152-7161
ISSN
  • 0021-8561 (ISSN-L)
  • 1520-5118
OpenAlex
W3037122402
Cited by
199
References
70
Citations by year
2026: 32 · 2025: 48 · 2024: 49 · 2023: 28 · 2022: 27 · 2021: 14 · 2020: 1
FWCI
10.68
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Agricultural and Food Chemistry (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Natural Science Foundation of China (81871094)
  • Basic & Public Welfare Research Foundation of Zhejiang (LGF18H090016)
  • Science & Technology Foundation of Wenzhou (Y20170065)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords
Alzheimer's disease, GPR41, neuroinflammation, microglial activation, amyloid-beta, cognitive impairment, cyclooxygenase-2, IL-1β, APP/PS1 mice, neuroprotection
MeSH terms
Acetates, Alzheimer Disease, Animals, Anti-Inflammatory Agents, Cognition, Fatty Acids, Volatile, Humans, Male, Mice, Transgenic, Up-Regulation, Amyloid beta-Peptides, NF-kappa B, Neuroprotective Agents, Receptors, G-Protein-Coupled, Extracellular Signal-Regulated MAP Kinases, MAP Kinase Kinase 4, Mice, Cyclooxygenase 2

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