Evidence map›Paper›PMID 27021024›Full record

ArticleMolecular neurobiology2017

Ginsenoside Reduces Cognitive Impairment During Chronic Cerebral Hypoperfusion Through Brain-Derived Neurotrophic Factor Regulated by Epigenetic Modulation.

Qun Wan, Xue Ma, Zhi-Jun Zhang, Ting Sun, Feng Xia, Gang Zhao, Yu-Mei Wu

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 3 pooled it
2.0field-weighted citation impact, top 14% 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

27 citing papers in PubMed, 3 syntheses or guidelines pooled it, 49 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Qun WanDepartment of Neurology, Xijing Hospital, the Fourth Military Medical University, Xi'an, Shaanxi Province, 710032, People's Republic of China.
Xue MaDepartment of Pharmacology, School of Pharmacy, The Fourth Military Medical University, Xi'an, Shaanxi Province, 710032, People's Republic of China.
Zhi-Jun ZhangDepartment of Neurology, Xijing Hospital, the Fourth Military Medical University, Xi'an, Shaanxi Province, 710032, People's Republic of China.
Ting SunDepartment of Pharmacology, School of Pharmacy, The Fourth Military Medical University, Xi'an, Shaanxi Province, 710032, People's Republic of China.
Feng XiaDepartment of Neurology, Xijing Hospital, the Fourth Military Medical University, Xi'an, Shaanxi Province, 710032, People's Republic of China.
Gang ZhaoDepartment of Neurology, Xijing Hospital, the Fourth Military Medical University, Xi'an, Shaanxi Province, 710032, People's Republic of China.
Yu-Mei WuDepartment of Pharmacology, School of Pharmacy, The Fourth Military Medical University, Xi'an, Shaanxi Province, 710032, People's Republic of China. yumeiwu@fmmu.edu.cn.
Air Force Medical University · CNXijing Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increased expression of brain-derived neurotrophic factor (BDNF) has been associated with memory-enhancing and neuroprotective properties of some drugs under chronic cerebral hypoperfusion (CCH) condition. Ginsenoside Rd (GSRd), one of the main active ingredients in Panax ginseng, is widely used for brain protection. However, it is poorly understood whether epigenetic mechanisms implied in the BDNF modulation after GSRd treatment for CCH remain elusive. Here, we investigated the neuroprotective effects of GSRd and the involved mechanisms. We demonstrated that GSRd administration ameliorated CCH-induced impairment of learning and memory behaviors, evidenced by decreased escape latency and increased number of crossing the platform in Morris water maze test. This improvement was associated with promoted neuron survival and increased BDNF expression in the hippocampus and prefrontal cortex of CCH mice. GSRd improved neuron survival and decreased neuron apoptosis and the level of caspase-3 under oxygen-glucose deprivation/reoxygenation (OGD/R) by upregulation of BDNF as well as in vitro. The levels of acetylated histone H3 (Ac-H3) and histone deacetylase (histone deacetylase 2 (HDAC2)) were altered under OGD/R in a time-dependent manner, and GSRd reestablished the balance between Ac-H3 and HDAC2 which resulted in upregulation of BDNF and increased neuron survival. MS-275, an inhibitor of class I HDACs, abolished the levels of Ac-H3 at the bdnf promoters and enhanced upregulation of BDNF after GSRd administration, suggesting a synergistic effect between GSRd and MS-275. All the data suggested that GSRd provided neuroprotection by epigenetic modulation which accounted for the regulation of BDNF in CCH mice.

Indexed as

Epigenesis, GeneticAcetylationAnimalsBrain-Derived Neurotrophic FactorBrain IschemiaCells, CulturedCell SurvivalChronic DiseaseCognitive DysfunctionCREB-Binding ProteinGinsenosidesGlucoseHippocampusHistone Deacetylase 2HistonesMaleBrain-Derived Neurotrophic FactorCREB-Binding Proteinginsenoside RdGinsenosidesGlucoseHistone Deacetylase 2HistonesOxygenp300-CBP-Associated Factorp300-CBP Transcription FactorsBrain-derived neurotrophic factorChronic cerebral hypoperfusionEpigeneticGinsenoside RdHDAC2Histone H3

Identifiers

PMID27021024
OpenAlexW2317998309

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.