Evidence map›Paper›PMID 23793904›Full record

ArticleNeurochemical research2013

Effect of HDAC inhibitors on neuroprotection and neurite outgrowth in primary rat cortical neurons following ischemic insult.

Mohammad Rakibul Hasan, Ji-Hye Kim, Youn Jung Kim, Kyoung Ja Kwon, Chan Young Shin, Hahn Young Kim, Seol-Heui Han, Dong-Hee Choi, Jongmin Lee

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

26 citing papers in PubMed, 42 citations in OpenAlex.

  1. The gut-brain axis: mechanisms linking intestinal dysbiosis with stroke.Frontiers in cell and developmental biology · 2026
    Review
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  8. Valproic Acid: A Potential Therapeutic for Spinal Cord Injury.Cellular and molecular neurobiology · 2021
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. HDAC Inhibitors InduceInternational journal of molecular sciences · 2019
    Article
  16. Article
  17. Review
  18. Dual mechanisms for the regulation of brain-derived neurotrophic factor by valproic acid in neural progenitor cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2018
    Article
  19. Article
  20. Article
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

9 authors at 2 institutions in 1 country.

Mohammad Rakibul HasanCenter for Neuroscience Research, SMART Institute of Advanced Biomedical Science, Konkuk University, Seoul, 143-701, Korea.
Ji-Hye Kim
Youn Jung Kim
Kyoung Ja Kwon
Chan Young Shin
Hahn Young Kim
Seol-Heui Han
Dong-Hee Choi
Jongmin Lee
Konkuk University · KRKyung Hee University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone deacetylase inhibitors (HDACi)-valproic acid (VPA) and trichostatin A (TSA) promote neurogenesis, neurite outgrowth, synaptic plasticity and neuroprotection. In this study, we investigated whether VPA and TSA promote post-ischemic neuroprotection and neuronal restoration in rat primary cortical neurons. On 6 days in vitro (DIV), cortical neurons were exposed to oxygen-glucose deprivation for 90 min. Cells were returned to normoxic conditions and cultured for 1, 3, or 7 days with or without VPA and TSA. Control cells were cultured in normoxic conditions only. On 7, 9, and 13 DIV, cells were measured neurite outgrowth using the Axiovision program and stained with Tunel staining kit. Microtubule associated protein-2 immunostaining and tunel staining showed significant recovery of neurite outgrowth and post-ischemic neuronal death by VPA or TSA treatment. We also determined levels of acetylated histone H3, PSD95, GAP 43 and synaptophysin. Significant increases in all three synaptic markers and acetylated histone H3 were observed relative to non-treated cells. Post-ischemic HDACi treatment also significantly raised levels of brain derived neurotrophic factor (BDNF) expression and secreted BDNF. Enhanced BDNF expression by HDACi treatment might have been involved in the post-ischemic neuroprotection and neuronal restorative effects. Our findings suggest that both VPA and TSA treatment during reoxygenation after ischemia may help post-ischemic neuroprotection and neuronal regeneration via increased BDNF expression and activation.

Indexed as

NeuritesAnimalsBase SequenceBrain-Derived Neurotrophic FactorDNA PrimersFemaleHistone Deacetylase InhibitorsNeuroprotective AgentsPregnancyRatsRats, Sprague-DawleyReverse Transcriptase Polymerase Chain ReactionBrain-Derived Neurotrophic FactorDNA PrimersHistone Deacetylase InhibitorsNeuroprotective Agents

Identifiers

PMID23793904
OpenAlexW1993499137

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.