Evidence map›Paper›PMID 30767185›Full record

ArticleMolecular neurobiology2019

Effect of the HDAC Inhibitor, Sodium Butyrate, on Neurogenesis in a Rat Model of Neonatal Hypoxia-Ischemia: Potential Mechanism of Action.

Joanna Jaworska, Teresa Zalewska, Joanna Sypecka, Malgorzata Ziemka-Nalecz

Open access · hybridAbstract read
In one paragraph

Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

71 citing papers in PubMed, 91 citations in OpenAlex.

  1. Review
  2. Perinatal lead (Pb) exposure and alterations to amyloid beta and metabolic profiles in the brain.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
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  8. The gut-brain axis: mechanisms linking intestinal dysbiosis with stroke.Frontiers in cell and developmental biology · 2026
    Review
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11 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Joanna JaworskaNeurorepair Department, Mossakowski Medical Research Centre, Polish Academy of Sciences, 5 A. Pawinskiego Street, 02-106, Warsaw, Poland.
Teresa ZalewskaNeurorepair Department, Mossakowski Medical Research Centre, Polish Academy of Sciences, 5 A. Pawinskiego Street, 02-106, Warsaw, Poland.
Joanna SypeckaNeurorepair Department, Mossakowski Medical Research Centre, Polish Academy of Sciences, 5 A. Pawinskiego Street, 02-106, Warsaw, Poland.
Malgorzata Ziemka-NaleczNeurorepair Department, Mossakowski Medical Research Centre, Polish Academy of Sciences, 5 A. Pawinskiego Street, 02-106, Warsaw, Poland. mnalecz@imdik.pan.pl.ORCID http://orcid.org/0000-0001-8412-995X
Mossakowski Medical Research Institute, Polish Academy of Sciences · PL

Funding

Narodowe Centrum Nauki 2015/17/N/NZ7/00969Narodowe Centrum Nauki 2017/27/B/NZ3/00582
6 · The paper itself

Abstract

Neonatal hypoxic-ischemic (HI) brain injury likely represents the major cause of long-term neurodevelopmental disabilities in surviving babies. Despite significant investigations, there is not yet any known reliable treatment to reduce brain damage in suffering infants. Our recent studies in an animal model of HI revealed the therapeutic potential of a histone deacetylase inhibitor (HDACi). The neuroprotective action was connected with the stimulation of neurogenesis in the dentate gyrus subgranular zone. In the current study, we investigated whether HDACi-sodium butyrate (SB)-would also lead to neurogenesis in the subventricular zone (SVZ). By using a neonatal rat model of hypoxia-ischemia, we found that SB treatment stimulated neurogenesis in the damaged ipsilateral side, based on increased DCX labeling, and restored the number of neuronal cells in the SVZ ipsilateral to lesioning. The neurogenic effect was associated with inhibition of inflammation, expressed by a transition of microglia to the anti-inflammatory phenotype (M2). In addition, the administration of SB increased the activation of the TrkB receptor and the phosphorylation of the transcription factor-CREB-in the ipsilateral hemisphere. In contrast, SB administration reduced the level of HI-induced p75

Indexed as

AcetylationAnimalsBrainButyric AcidCell ProliferationCyclic AMP Response Element-Binding ProteinDisease Models, AnimalDoublecortin ProteinHistone Deacetylase InhibitorsHypoxia-Ischemia, BrainMacrophagesMAP Kinase Signaling SystemMicrogliaNerve Growth FactorsNeurogenesisOligodendrogliaButyric AcidCyclic AMP Response Element-Binding ProteinDcx protein, ratDoublecortin ProteinHistone Deacetylase InhibitorsNerve Growth FactorsProto-Oncogene Proteins c-aktReceptors, Nerve Growth FactorTubulinBDNF–TrkB pathwayCREBERK kinaseNeonatal hypoxia–ischemiaNeurogenesis

Identifiers

PMID30767185
PMCPMC6682584
OpenAlexW2914227839

What Socratic 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 Socratic graph.