Evidence map›Paper›PMID 21671257›Full record

ArticleJournal of neuroscience research2011

Cyanidin-3-glucoside ameliorates ethanol neurotoxicity in the developing brain.

Zunji Ke, Ying Liu, Xin Wang, Zhiqin Fan, Gang Chen, Mei Xu, Kimberley A Bower, Jacqueline A Frank, Xiaoming Ou, Xianglin Shi and 1 more

Open access · greenAbstract read
In one paragraph

Article in Journal of neuroscience research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
6.6field-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

24 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
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  9. Article
  10. Role of MCP-1 and CCR2 in alcohol neurotoxicity.Pharmacological research · 2019
    Review
  11. Cyanidin-3-glucoside inhibits amyloid βThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2018
    Article
  12. Article
  13. Review
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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

11 authors at 4 institutions in 2 countries.

Zunji KeDepartment of Internal Medicine, University of Kentucky College of Medicine, Lexington, Kentucky 40536, USA.
Ying Liu
Xin Wang
Zhiqin Fan
Gang Chen
Mei Xu
Kimberley A Bower
Jacqueline A Frank
Xiaoming Ou
Xianglin Shi
Jia Luo
University of Kentucky · USChinese Academy of Sciences · CNShanghai Institutes for Biological Sciences · CNUniversity of Mississippi Medical Center · US

Funding

GSK3BETA, A MEDIATOR OF ETHANOL NEUROTOXICITYR01AA015407 · NIAAA · WEST VIRGINIA UNIVERSITY · PI JIA LUO · 2005 to 2026
$6.2M
Autophagic Protection of Ethanol NeurotoxicityR21AA019693 · NIAAA · UNIVERSITY OF KENTUCKY · PI LUO, JIA · 2010 to 2011
$392k
NIAAA NIH HHS AA015407NIAAA NIH HHS AA019693NIAAA NIH HHS R01 AA015407NIAAA NIH HHS R21 AA019693
6 · The paper itself

Abstract

Ethanol exposure induces neurodegeneration in the developing central nervous system (CNS). Fetal alcohol spectrum disorders (FASD) are caused by ethanol exposure during pregnancy and are the most common nonhereditary cause of mental retardation. It is important to identify agents that provide neuroprotection against ethanol neurotoxicity. Multiple mechanisms have been proposed for ethanol-induced neurodegeneration, and oxidative stress is one of the most important mechanisms. Recent evidence indicates that glycogen synthase kinase 3β (GSK3β) is a potential mediator of ethanol-mediated neuronal death. Cyanidin-3-glucoside (C3G), a member of the anthocyanin family, is a potent natural antioxidant. Our previous study suggested that C3G inhibited GSK3β activity in neurons. Using a third trimester equivalent mouse model of ethanol exposure, we tested the hypothesis that C3G can ameliorate ethanol-induced neuronal death in the developing brain. Intraperitoneal injection of C3G reduced ethanol-meditated caspase-3 activation, neurodegeneration, and microglial activation in the cerebral cortex of 7-day-old mice. C3G blocked ethanol-mediated GSK3β activation by inducing phosphorylation at serine 9 while reducing the phosphorylation at tyrosine 216. C3G also inhibited ethanol-stimulated expression of malondialdehyde (MDA) and p47phox, indicating that C3G alleviated ethanol-induced oxidative stress. These results provide important insight into the therapeutic potential of C3G.

Indexed as

Alcohol-Induced Disorders, Nervous SystemAnimalsAnthocyaninsBrainDisease Models, AnimalEthanolFemaleFetal Alcohol Spectrum DisordersGlucosidesMiceMice, Inbred C57BLNeuroprotective AgentsPregnancyAnthocyaninscyanidin-3-O-beta-glucopyranosideEthanolGlucosidesNeuroprotective Agents

Identifiers

PMID21671257
PMCPMC3154369
OpenAlexW2111816207

What OpenQuestion holds

Textmetadata
LicenceTDM
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.