Evidence map›Paper›PMID 19291322›Full record

ArticleJournal of neuroinflammation2009

Acetaminophen inhibits neuronal inflammation and protects neurons from oxidative stress.

Debjani Tripathy, Paula Grammas

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
9.2field-weighted citation impact, top 2% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

  1. Pooled it
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  16. Ethanol extracts fromAmerican journal of translational research · 2016
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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 2 institutions in 1 country.

Debjani TripathyGarrison Institute on Aging, Department of Neurology, Texas Tech University Health Sciences Center, Lubbock, Texas, USA. debjani.tripathy@ttuhsc.edu
Paula Grammas
Texas Tech University · USTexas Tech University Health Sciences Center · US

Funding

VASCULAR-MEDIATED NEURONAL CELL DEATH IN ALZHEIMER'SR01AG015964 · NIA · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI GRAMMAS, PAULA · 1999 to 2011
$2.5M
Vascular inflammation and neurotoxicity in aging brainR01AG028367 · NIA · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI GRAMMAS, PAULA · 2006 to 2009
$1.3M
Is There a Link Between Alzheimer's and AtherosclerosisR01AG020569 · NIA · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI GRAMMAS, PAULA · 2004 to 2007
$1.3M
NIA NIH HHS AG020569NIA NIH HHS AG028367NIA NIH HHS AG15964NIA NIH HHS R01 AG015964NIA NIH HHS R01 AG020569NIA NIH HHS R01 AG028367
6 · The paper itself

Abstract

backgroundRecent studies have demonstrated a link between the inflammatory response, increased cytokine formation, and neurodegeneration in the brain. The beneficial effects of anti-inflammatory drugs in neurodegenerative diseases, such as Alzheimer's disease (AD), have been documented. Increasing evidence suggests that acetaminophen has unappreciated anti-oxidant and anti-inflammatory properties. The objectives of this study are to determine the effects of acetaminophen on cultured brain neuronal survival and inflammatory factor expression when exposed to oxidative stress.

methodsCerebral cortical cultured neurons are pretreated with acetaminophen and then exposed to the superoxide-generating compound menadione (5 microM). Cell survival is assessed by MTT assay and inflammatory protein (tumor necrosis factor alpha, interleukin-1, macrophage inflammatory protein alpha, and RANTES) release quantitated by ELISA. Expression of pro- and anti-apoptotic proteins is assessed by western blots.

resultsAcetaminophen has pro-survival effects on neurons in culture. Menadione, a superoxide releasing oxidant stressor, causes a significant (p < 0.001) increase in neuronal cell death as well as in the release of tumor necrosis factor alpha, interleukin-1, macrophage inflammatory protein alpha, and RANTES from cultured neurons. Pretreatment of neuronal cultures with acetaminophen (50 microM) increases neuronal cell survival and inhibits the expression of these cytokines and chemokines. In addition, we document, for the first time, that acetaminophen increases expression of the anti-apoptotic protein Bcl2 in brain neurons and decreases the menadione-induced elevation of the proapoptotic protein, cleaved caspase 3. We show that blocking acetaminophen-induced expression of Bcl2 reduces the pro-survival effect of the drug.

conclusionThese data show that acetaminophen has anti-oxidant and anti-inflammatory effects on neurons and suggest a heretofore unappreciated therapeutic potential for this drug in neurodegenerative diseases such as AD that are characterized by oxidant and inflammatory stress.

Indexed as

AcetaminophenAnalysis of VarianceAnimalsAnti-Inflammatory Agents, Non-SteroidalAntioxidantsApoptosisbcl-Associated Death ProteinBlotting, WesternCells, CulturedCell SurvivalCerebral CortexChemokinesCytokinesNeuronsOxidantsOxidative StressAcetaminophenAnti-Inflammatory Agents, Non-SteroidalAntioxidantsbcl-Associated Death ProteinChemokinesCytokinesOxidantsRNA, Small InterferingVitamin K 3

Identifiers

PMID19291322
PMCPMC2662814
OpenAlexW2098629559

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.