Evidence map›Paper›PMID 27193049›Full record

ArticleBMC neuroscience2016

Histone deacetylase inhibitor SAHA attenuates post-seizure hippocampal microglia TLR4/MYD88 signaling and inhibits TLR4 gene expression via histone acetylation.

Qing-Peng Hu, Ding-An Mao

Open access · goldAbstract read
In one paragraph

Article in BMC neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
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  4. Post-translational modifications regulating microglial inflammation in central nervous system disorders: a review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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  13. Impact of Stress on Epilepsy: Focus on Neuroinflammation-A Mini Review.International journal of molecular sciences · 2021
    Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. TheAnnals of translational medicine · 2020
    Article
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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.

Qing-Peng HuDepartment of Pediatrics, The Second Xiang-Ya Hospital, Central South University, 139 Middle Renmin Road, Changsha, 410011, Hunan, China.
Ding-An MaoDepartment of Pediatrics, The Second Xiang-Ya Hospital, Central South University, 139 Middle Renmin Road, Changsha, 410011, Hunan, China. ma_jinan@yahoo.com.
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEpilepsy is a common neurological disorder characterized by recurrent unprovoked seizures. Seizure-induced TLR4/MYD88 signaling plays a critical role in activating microglia and triggering neuron apoptosis. SAHA is a histone deacetylase inhibitor that regulates gene expression by increasing chromatin histone acetylation. In this study, we investigated the role of SAHA in TLR4/MYD88 signaling in a rat seizure model.

resultsSprague-Dawley rats with kainic acid (KA)-induced seizures were treated with SAHA. The expression of TLR4, MYD88, NF-κB P65 and IL-1β in hippocampus was detected at hour 2 and 6 and day 1, 2, and 3 post seizure. SAHA pretreatment increased seizure latency and decreased seizure scores. The expression levels of TLR4, MYD88, NF-κB and IL-1β increased significantly in both activated microglia and apoptotic neurons after KA treatment. The effects were attenuated by SAHA. Chromatin immunoprecipitation assays indicated that the H3 histone acetylation levels significantly decreased while H3K9 levels significantly increased in the KA treatment group. The H3 and H3K9 acetylation levels returned to control levels after SAHA (50 mg/kg) pretreatment. There was a positive correlation between the expression of TLR4 and the acetylation levels of H3K9.

conclusionsHistone deacetylase inhibitor SAHA can suppress seizure-induced TLR4/MYD88 signaling and inhibit TLR4 gene expression through histone acetylation regulation. This suggests that SAHA may protect against seizure-induced brain damage.

Indexed as

AcetylationAnimalsAnticonvulsantsApoptosisCA1 Region, HippocampalDisease Models, AnimalDose-Response Relationship, DrugGene ExpressionHistone Deacetylase InhibitorsHistonesHydroxamic AcidsKainic AcidMaleMicrogliaMyeloid Differentiation Factor 88NeuronsAnticonvulsantsHistone Deacetylase InhibitorsHistonesHydroxamic AcidsKainic AcidMyd88 protein, mouseMyeloid Differentiation Factor 88Tlr4 protein, mouseToll-Like Receptor 4VorinostatHistone acetylationHistone deacetylaseMicrogliaMYD88SAHASeizuresToll-like-receptor 4 (TLR4)

Identifiers

PMID27193049
PMCPMC4872358
OpenAlexW2407650432

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.