Evidence map›Paper›PMID 42700316›Full record

ArticleMolecular biology reports2026

Ellagic acid regulates astrocytic responses under inflammatory conditions in primary astrocyte cultures: effects on oxidative stress, inflammatory cytokines, and glycogen synthase kinase-3β.

Thais Marini da Rosa, Larissa Menezes da Silveira, Natália Pontes Bona, Juliane Torchelsen Saraiva, Júlia Araújo da Silva, William Borges Domingues, Lucas Petitemberte de Souza, Mariana Cavalcanti Nascimento, Vinicius Farias Campos, Francieli Moro Stefanello and 3 more

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In one paragraph

Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Thais Marini da RosaPrograma de Pós-Graduação em Bioquímica e Bioprospecção, Universidade Federal de Pelotas, Campus Universitário Capão do Leão s/n, Pelotas, RS, CEP 96010-900, Brazil.
Larissa Menezes da SilveiraPrograma de Pós-Graduação em Bioquímica e Bioprospecção, Universidade Federal de Pelotas, Campus Universitário Capão do Leão s/n, Pelotas, RS, CEP 96010-900, Brazil.
Natália Pontes BonaPrograma de Pós-Graduação em Bioquímica e Bioprospecção, Universidade Federal de Pelotas, Campus Universitário Capão do Leão s/n, Pelotas, RS, CEP 96010-900, Brazil.
Juliane Torchelsen SaraivaPrograma de Pós-Graduação em Bioquímica e Bioprospecção, Universidade Federal de Pelotas, Campus Universitário Capão do Leão s/n, Pelotas, RS, CEP 96010-900, Brazil.
Júlia Araújo da SilvaPrograma de Pós-Graduação em Bioquímica e Bioprospecção, Universidade Federal de Pelotas, Campus Universitário Capão do Leão s/n, Pelotas, RS, CEP 96010-900, Brazil.
William Borges DominguesPrograma de Pós-Graduação em Biotecnologia, Universidade Federal de Pelotas, Campus Universitário Capão do Leão, s/n, Pelotas, RS, CEP 96010-900, Brazil.
Lucas Petitemberte de SouzaPrograma de Pós-Graduação em Biotecnologia, Universidade Federal de Pelotas, Campus Universitário Capão do Leão, s/n, Pelotas, RS, CEP 96010-900, Brazil.
Mariana Cavalcanti NascimentoPrograma de Pós-Graduação em Biotecnologia, Universidade Federal de Pelotas, Campus Universitário Capão do Leão, s/n, Pelotas, RS, CEP 96010-900, Brazil.
Vinicius Farias CamposPrograma de Pós-Graduação em Bioquímica e Bioprospecção, Universidade Federal de Pelotas, Campus Universitário Capão do Leão s/n, Pelotas, RS, CEP 96010-900, Brazil.
Francieli Moro StefanelloPrograma de Pós-Graduação em Bioquímica e Bioprospecção, Universidade Federal de Pelotas, Campus Universitário Capão do Leão s/n, Pelotas, RS, CEP 96010-900, Brazil.
Cinthia Melazzo de AndradePrograma de Pós-Graduação em Medicina Veterinária, Universidade Federal de Santa Maria, Cidade Universitária, Santa Maria, RS, CEP 97105-900, Brazil.
Nathalia Stark PedraPrograma de Pós-Graduação em Bioquímica e Bioprospecção, Universidade Federal de Pelotas, Campus Universitário Capão do Leão s/n, Pelotas, RS, CEP 96010-900, Brazil.
Roselia Maria SpanevelloPrograma de Pós-Graduação em Bioquímica e Bioprospecção, Universidade Federal de Pelotas, Campus Universitário Capão do Leão s/n, Pelotas, RS, CEP 96010-900, Brazil. roselia.spanevello@ufsm.br.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeuroinflammation involves the activation of glial cells, particularly astrocytes, and microglia, in response to pathological stimuli. Astrocyte activation is characterized by increased pro-inflammatory cytokines and oxidative stress. Given their role in neuroinflammation, targeting astrocytic mechanisms presents potential therapeutic opportunities. Ellagic acid (EA), a phenolic compound, exhibits antioxidant, anti-inflammatory, and neuroprotective effects. This study investigated the effect of EA on astrocytes from neonatal rats exposed to lipopolysaccharide (LPS), a potent proinflammatory agent widely used to induce neuroinflammation in vitro. METHODS AND

resultsAstrocytes were pretreated with EA (50, 100, and 200 µM) for 48 h and subsequently exposed to LPS (1 µg/mL) for 3h. Cell viability and proliferation, inflammatory and oxidative stress parameters were evaluated. LPS decreased astrocytic viability and increased cell proliferation and EA prevented these alterations. EA also attenuated the LPS-induced increase in reactive oxygen species and nitrite levels and the decrease in sulfhydryl content and antioxidant enzyme activities. LPS induced an increase in gene expression of interleukin 1β and tumor necrosis factor-alpha, and EA treatment attenuated these alterations. Conversely, EA increased interleukin 6 (IL-6) and glycogen synthase kinase-3 beta mRNA expression compared with LPS-only exposure. LPS increased IL-6 levels and decreased interleukin 10 (IL-10) levels in astrocytes, and EA at 100 µM prevented the reduction in IL-10 levels but did not significantly modify IL-6 levels compared with LPS group.

conclusionEA modulates oxidative and inflammatory markers in LPS-stimulated astrocytes. Further studies are needed to clarify the underlying mechanisms and evaluate these effects in more complex models of neuroinflammation.

Indexed as

AstrocytesEllagic AcidGlycogen Synthase Kinase 3 betaAnimalsAntioxidantsCell ProliferationCells, CulturedCell SurvivalCytokinesInflammationLipopolysaccharidesNeuroinflammatory DiseasesOxidative StressRatsReactive Oxygen SpeciesAntioxidantsCytokinesEllagic AcidGlycogen Synthase Kinase 3 betaGsk3b protein, ratLipopolysaccharidesReactive Oxygen SpeciesAntioxidantAstrocytesEllagic acidGSK-3βInterleukinLipopolysaccharideNeuroinflammation

Identifiers

PMID42700316
PMCPMC13546155

What Socratic holds

Textmetadata
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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 Socratic graph.