Evidence map›Paper›PMID 30529756›Full record

ArticleAlcohol (Fayetteville, N.Y.)2019

Minocycline attenuates ethanol-induced cell death and microglial activation in the developing spinal cord.

Zhenhua Ren, Xin Wang, Mei Xu, Jacqueline A Frank, Jia Luo

Open access · greenAbstract read
In one paragraph

Article in Alcohol (Fayetteville, N.Y.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

13 citing papers in PubMed, 22 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

5 authors at 3 institutions in 2 countries.

Zhenhua RenDepartment of Anatomy, School of Basic Medicine, Anhui Medical University, Hefei, Anhui, 230032, China; Department of Pharmacology and Nutritional Sciences, University of Kentucky College of Medicine, Lexington, KY 40536, United States.
Xin WangDepartment of Pharmacology and Nutritional Sciences, University of Kentucky College of Medicine, Lexington, KY 40536, United States.
Mei XuDepartment of Pharmacology and Nutritional Sciences, University of Kentucky College of Medicine, Lexington, KY 40536, United States.
Jacqueline A FrankDepartment of Pharmacology and Nutritional Sciences, University of Kentucky College of Medicine, Lexington, KY 40536, United States.
Jia LuoDepartment of Pharmacology and Nutritional Sciences, University of Kentucky College of Medicine, Lexington, KY 40536, United States; Lexington Veterans Administration Health Care System, Research & Development, 1101 Veterans Drive, Lexington, KY 40502, United States. Electronic address: jialuo888@uky.edu.
University of Kentucky · USAnhui Medical University · CNLexington VA Health Care System · US

Funding

GSK3BETA, A MEDIATOR OF ETHANOL NEUROTOXICITYR01AA015407 · NIAAA · WEST VIRGINIA UNIVERSITY · PI JIA LUO · 2005 to 2026
$6.2M
ALCOHOL AND BREAST CANCERR01AA017226 · NIAAA · WEST VIRGINIA UNIVERSITY · PI LUO, JIA · 2008 to 2024
$5.2M
Thiamine deficiency and alcohol-induced neurodegenerationI01BX001721 · VA · VA MEDICAL CENTER - LEXINGTON, KY · PI LUO, JIA · 2014 to 2022
–
BLRD VA I01 BX001721NIAAA NIH HHS R01 AA015407NIAAA NIH HHS R01 AA017226
6 · The paper itself

Abstract

Developmental exposure to ethanol may cause fetal alcohol spectrum disorders (FASD), and the immature central nervous system (CNS) is particularly vulnerable to ethanol. In addition to vulnerability in the developing brain, we previously showed that ethanol also caused neuroapoptosis, microglial activation, and neuroinflammation in the spinal cord. Minocycline is an antibiotic that inhibits microglial activation and alleviates neuroinflammation. We sought to determine whether minocycline could protect spinal cord neurons against ethanol-induced damage. In this study, we showed that minocycline significantly inhibited ethanol-induced caspase-3 activation, microglial activation, and the expression of pro-inflammatory cytokines in the developing spinal cord. Moreover, minocycline blocked ethanol-induced activation of glycogen synthase kinase 3 beta (GSK3β), a key regulator of microglial activation. Meanwhile, minocycline significantly restored ethanol-induced inhibition of protein kinase B (AKT), mammalian target of the rapamycin (mTOR), and ERK1/2 signaling pathways, which were important pro-survival signaling pathways for neurons. Together, minocycline may attenuate ethanol-induced damage to the developing spinal cord by inhibiting microglial activation/neuroinflammation and by restoring the pro-survival signaling.

Indexed as

AnimalsAnti-Bacterial AgentsApoptosisCaspase 3CytokinesEthanolFemaleGlycogen Synthase Kinase 3 betaMaleMAP Kinase Signaling SystemMiceMicrogliaMinocyclineNeurogenic InflammationProto-Oncogene Proteins c-aktSpinal CordAnti-Bacterial AgentsCaspase 3CytokinesEthanolGlycogen Synthase Kinase 3 betaGsk3b protein, mouseMinocyclinemTOR protein, mouseProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAlcoholFetal alcohol spectrum disordersGlycogen synthase kinase 3InflammationNeuroprotection

Identifiers

PMID30529756
PMCPMC6555701
OpenAlexW2904404809

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.