Evidence map›Paper›PMID 22528839›Full record

ArticleNeurochemical research2012

Gemfibrozil, a lipid lowering drug, inhibits the activation of primary human microglia via peroxisome proliferator-activated receptor β.

Malabendu Jana, Kalipada Pahan

Open access · greenAbstract read
In one paragraph

Article in Neurochemical research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

22 citing papers in PubMed, 27 citations in OpenAlex.

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  11. Activation of PPARα Exhibits Therapeutic Efficacy in a Mouse Model of Juvenile Neuronal Ceroid Lipofuscinosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  12. Gemfibrozil Protects Dopaminergic Neurons in a Mouse Model of Parkinson's Disease via PPARα-Dependent Astrocytic GDNF Pathway.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
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  15. Aspirin Induces Lysosomal Biogenesis and Attenuates Amyloid Plaque Pathology in a Mouse Model of Alzheimer's Disease via PPARα.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
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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

2 authors at 1 institution in 1 country.

Malabendu JanaDepartment of Neurological Sciences, Rush University Medical Center, 1735 West Harrison St., Suite 320, Chicago, IL 60612, USA.
Kalipada Pahan
Rush University Medical Center · US

Funding

Cinnamon, CNTF and EAER01AT006681 · NCCIH · RUSH UNIVERSITY MEDICAL CENTER · PI PAHAN, KALIPADA · 2011 to 2015
$1.8M
NEMO-binding domain peptide in a monkey model of PDR21NS064564 · NINDS · RUSH UNIVERSITY MEDICAL CENTER · PI PAHAN, KALIPADA · 2010 to 2011
$410k
Castration of male mice: An unexpected way to model PD pathologiesR21NS071479 · NINDS · RUSH UNIVERSITY MEDICAL CENTER · PI PAHAN, KALIPADA · 2010 to 2011
$409k
NCCIH NIH HHS AT6681NCCIH NIH HHS R01 AT006681NINDS NIH HHS NS64564NINDS NIH HHS NS71479NINDS NIH HHS R21 NS064564NINDS NIH HHS R21 NS071479
6 · The paper itself

Abstract

Microglial activation participates in the pathogenesis of various neuroinflammatory and neurodegenerative diseases. However, mechanisms by which microglial activation could be controlled are poorly understood. Peroxisome proliferator-activated receptors (PPAR) are transcription factors belonging to the nuclear receptor super family with diverse effect. This study underlines the importance of PPARβ/δ in mediating the anti-inflammatory effect of gemfibrozil, an FDA-approved lipid-lowering drug, in primary human microglia. Bacterial lipopolysachharides (LPS) induced the expression of various proinflammatory molecules and upregulated the expression of microglial surface marker CD11b in human microglia. However, gemfibrozil markedly suppressed proinflammatory molecules and CD11b in LPS-stimulated microglia. Human microglia expressed PPAR-β and -γ, but not PPAR-α. Interestingly, either antisense knockdown of PPAR-β or antagonism of PPAR-β by a specific chemical antagonist abrogated gemfibrozil-mediated inhibition of microglial activation. On the other hand, blocking of PPAR-α and -γ had no effect on gemfibrozil-mediated anti-inflammatory effect in microglia. These results highlight the fact that gemfibrozil regulates microglial activation by inhibiting inflammatory gene expression in a PPAR-β dependent pathway and further reinforce its therapeutic application in several neuroinflammatory and neurodegenerative diseases.

Indexed as

CD11b AntigenGemfibrozilHumansInterleukin-6LipopolysaccharidesMicrogliaNitric Oxide Synthase Type IIPPAR-betaPPAR gammaCD11b AntigenGemfibrozilInterleukin-6ITGAM protein, humanLipopolysaccharidesNitric Oxide Synthase Type IINOS2 protein, humanPPAR-betaPPAR gamma

Identifiers

PMID22528839
PMCPMC3389313
OpenAlexW2007257049

What OpenQuestion holds

Textmetadata
LicenceTDM
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.