Evidence map›Paper›PMID 29947014›Full record

ArticleNeurochemical research2018

Lauric Acid Alleviates Neuroinflammatory Responses by Activated Microglia: Involvement of the GPR40-Dependent Pathway.

Yasunori Nishimura, Mitsuaki Moriyama, Kenji Kawabe, Hideyo Satoh, Katsura Takano, Yasu-Taka Azuma, Yoichi Nakamura

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.7field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 52 citations in OpenAlex.

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  5. Article
  6. Carboxylic Acids as Activators of NRF2: Antioxidant and Anti-inflammatory Effects.Medicinal chemistry (Shariqah (United Arab Emirates)) · 2025
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Yasunori NishimuraLaboratory of Integrative Physiology in Veterinary Sciences, Osaka Prefecture University, 1-58 Rinku-Ourai Kita, Izumisano, Osaka, 598-8531, Japan.
Mitsuaki MoriyamaLaboratory of Integrative Physiology in Veterinary Sciences, Osaka Prefecture University, 1-58 Rinku-Ourai Kita, Izumisano, Osaka, 598-8531, Japan. moriyama@vet.osakafu-u.ac.jp.ORCID http://orcid.org/0000-0001-8123-8835
Kenji KawabeLaboratory of Integrative Physiology in Veterinary Sciences, Osaka Prefecture University, 1-58 Rinku-Ourai Kita, Izumisano, Osaka, 598-8531, Japan.
Hideyo SatohLaboratory of Integrative Physiology in Veterinary Sciences, Osaka Prefecture University, 1-58 Rinku-Ourai Kita, Izumisano, Osaka, 598-8531, Japan.
Katsura TakanoLaboratory of Integrative Physiology in Veterinary Sciences, Osaka Prefecture University, 1-58 Rinku-Ourai Kita, Izumisano, Osaka, 598-8531, Japan.
Yasu-Taka AzumaLaboratory of Veterinary Pharmacology, Osaka Prefecture University, Izumisano, Osaka, Japan.
Yoichi NakamuraLaboratory of Integrative Physiology in Veterinary Sciences, Osaka Prefecture University, 1-58 Rinku-Ourai Kita, Izumisano, Osaka, 598-8531, Japan.
Osaka Prefecture University · JP

Funding

Japan Society for the Promotion of Science (JP) KAKENHI 15K07768Japan Society for the Promotion of Science (JP) KAKENHI 17K08127Japan Society for the Promotion of Science (JP) KAKENHI 17K15390
6 · The paper itself

Abstract

In several neurodegenerative diseases such as Alzheimer's disease (AD), microglia are hyperactivated and release nitric oxide (NO) and proinflammatory cytokines, resulting its neuropathology. Mounting evidence indicates that dietary supplementation with coconut oil (CNO) reduces the cognitive deficits associated with AD; however, the precise mechanism(s) underlying the beneficial effect of CNO are unknown. In the present study, we examined the effects of lauric acid (LA), a major constituent of CNO, on microglia activated experimentally by lipopolysaccharide (LPS), using primary cultured rat microglia and the mouse microglial cell line, BV-2. LA attenuated LPS-stimulated NO production and the expression of inducible NO synthase protein without affecting cell viability. In addition, LA suppressed LPS-induced reactive oxygen species and proinflammatory cytokine production, as well as phosphorylation of p38-mitogen activated protein kinase and c-Jun N-terminal kinase. LA-induced suppression of NO production was partially but significantly reversed in the presence of GW1100, an antagonist of G protein-coupled receptor (GPR) 40, which is an LA receptor on the plasma membrane. LA also decreased LPS-induced phagocytosis, which was completely reversed by co-treatment with GW1100. Moreover, LA alleviated amyloid-β-induced enhancement of phagocytosis. These results suggest that attenuation of microglial activation by LA may occur via the GPR40-dependent pathway. Such effects of LA may reduce glial activation and the subsequent neuronal damage in AD patients who consume CNO.

Indexed as

AnimalsCell LineCoconut OilCytokinesLauric AcidsLipopolysaccharidesMacrophage ActivationMacrophagesMicrogliaNitric OxidePhosphorylationRats, WistarReactive Oxygen SpeciesReceptors, G-Protein-CoupledCoconut OilCytokinesG-protein-coupled receptor 40, ratlauric acidLauric AcidsLipopolysaccharidesNitric OxideReactive Oxygen SpeciesReceptors, G-Protein-CoupledCoconut oilGPR40Lauric acidMicrogliaNeuroinflammationPhagocytosis

Identifiers

PMID29947014
OpenAlexW2810968975

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.