Evidence map›Paper›PMID 30906786›Full record

ArticleJournal of diabetes research2019

Inhibition of HDAC3 Ameliorates Cerebral Ischemia Reperfusion Injury in Diabetic Mice In Vivo and In Vitro.

Bo Zhao, Quan Yuan, Jia-Bao Hou, Zhong-Yuan Xia, Li-Ying Zhan, Mei Li, Meng Jiang, Wen-Wei Gao, Lian Liu

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
5.0field-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

33 citing papers in PubMed, 61 citations in OpenAlex.

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  10. The role of histone deacetylase 3 in breast cancer.Medical oncology (Northwood, London, England) · 2022
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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

9 authors at 1 institution in 1 country.

Bo ZhaoDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province 430060, China.
Quan YuanDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province 430060, China.
Jia-Bao HouDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province 430060, China.
Zhong-Yuan XiaDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province 430060, China.ORCID 0000-0002-5807-9554
Li-Ying ZhanDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province 430060, China.
Mei LiDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province 430060, China.
Meng JiangDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province 430060, China.
Wen-Wei GaoDepartment of Critical Care Medicine, Renmin Hospital of Wuhan University, Wuhan, Hubei Province 430060, China.ORCID 0000-0003-4405-0168
Lian LiuDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province 430060, China.ORCID 0000-0003-4861-9219
Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundA substantial increase in histone deacetylase 3 (HDAC3) expression is implicated in the pathological process of diabetes and stroke. However, it is unclear whether HDAC3 plays an important role in diabetes complicated with stroke. We aimed to explore the role and the potential mechanisms of HDAC3 in cerebral ischemia/reperfusion (I/R) injury in diabetic state.

methodsDiabetic mice were subjected to 1 h ischemia, followed by 24 h reperfusion. PC12 cells were exposed to high glucose for 24 h, followed by 3 h of hypoxia and 6 h of reoxygenation (H/R). Diabetic mice received RGFP966 (the specific HDAC3 inhibitor) or vehicle 30 minutes before the middle cerebral artery occlusion (MCAO), and high glucose-incubated PC12 cells were pretreated with RGFP966 or vehicle 6 h before H/R.

resultsHDAC3 inhibition reduced the cerebral infarct volume, ameliorated pathological changes, improved the cell viability and cytotoxicity, alleviated apoptosis, attenuated oxidative stress, and enhanced autophagy in cerebral I/R injury model in diabetic state in vivo and in vitro. Furthermore, we found that the expression of HDAC3 was remarkably amplified, and the Bmal1 expression was notably decreased in diabetic mice with cerebral I/R, whereas this phenomenon was obviously reversed by RGFP966 pretreatment.

conclusionsThese results suggested that the HDAC3 was involved in the pathological process of the complex disease of diabetic stroke. Suppression of HDAC3 exerted protective effects against cerebral I/R injury in diabetic state in vivo and in vitro via the modulation of oxidative stress, apoptosis, and autophagy, which might be mediated by the upregulation of Bmal1.

Indexed as

AnimalsApoptosisCell HypoxiaCell SurvivalDiabetes Mellitus, ExperimentalDisease Models, AnimalHistone Deacetylase InhibitorsMaleMalondialdehydeMiceNeuroprotective AgentsOxidative StressPC12 CellsRatsReactive Oxygen SpeciesReperfusion InjuryHistone Deacetylase InhibitorsMalondialdehydeNeuroprotective AgentsReactive Oxygen SpeciesSuperoxide Dismutase

Identifiers

PMID30906786
PMCPMC6393870
OpenAlexW2914822747

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Registered trials

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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.