Evidence map›Paper›PMID 32048246›Full record

ArticlePharmacological reports : PR2020

Metformin accelerates myelin recovery and ameliorates behavioral deficits in the animal model of multiple sclerosis via adjustment of AMPK/Nrf2/mTOR signaling and maintenance of endogenous oligodendrogenesis during brain self-repairing period.

Nima Sanadgol, Mahmood Barati, Fariba Houshmand, Shokoufeh Hassani, Tim Clarner, Mohsen Shahlaei, Fereshteh Golab

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Article in Pharmacological reports : PR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 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 6 institutions in 2 countries.

Nima SanadgolDepartment of Biology, Faculty of Sciences, University of Zabol, Zabol, Iran.
Mahmood BaratiDepartment of Biotechnology, Faculty of Allied Medicine, Iran University of Medical Science, Tehran, Iran.
Fariba HoushmandDepartment of Physiology, School of Medicine, Shahrekord University of Medical Sciences, Shahrekord, Iran.
Shokoufeh HassaniToxicology and Diseases Group, Institute of Pharmaceutical Sciences (TIPS), Tehran University of Medical Sciences, Tehran, Iran.
Tim ClarnerInstitute of Neuroanatomy, Faculty of Medicine, RWTH Aachen University, 52074, Aachen, Germany.
Mohsen ShahlaeiNano Drug Delivery Research Center, School of Pharmacy, Kermanshah University of Medical Science, Kermanshah, Iran.
Fereshteh GolabCellular and Molecular Research Center, Iran University of Medical Science, P.O. Box 14155-6451, Tehran, Iran. fgolab520@gmail.com.
Iran University of Medical Sciences · IRKermanshah University of Medical Sciences · IRRWTH Aachen University · DEShahrekord University of Medical Sciences · IRTehran University of Medical Sciences · IRZabol University · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMultiple sclerosis (MS) is a devastating autoimmune disorder characterized by oligodendrocytes (OLGs) loss and demyelination. In this study, we have examined the effects of metformin (MET) on the oligodendrogenesis, redox signaling, apoptosis, and glial responses during a self-repairing period (1-week) in the animal model of MS.

methodsFor induction of demyelination, C57BL/6 J mice were fed a 0.2% cuprizone (CPZ) for 5 weeks. Thereafter, CPZ was removed for 1-week and molecular and behavioral changes were monitored in the presence or absence of MET (50 mg/kg body weight/day).

resultsMET remarkably increased the localization of precursor OLGs (NG2

conclusionsAltogether, our study reveals that MET effectively induces lesion reduction and elevated molecular processes that support myelin recovery via direct activation of AMPK and indirect regulation of AMPK/Nrf2/mTOR pathway in OLGs. These findings facilitate the development of new therapeutic strategies based on AMPK activation for MS in the near future.

Indexed as

AMP-Activated Protein KinasesAnimalsApoptosisCorpus CallosumMaleMetforminMiceMice, Inbred C57BLMolecular Docking SimulationMotor ActivityMultiple SclerosisMyelin SheathNF-E2-Related Factor 2OligodendrogliaOxidantsSignal TransductionAMP-Activated Protein KinasesMetforminmTOR protein, mouseNfe2l2 protein, mouseNF-E2-Related Factor 2OxidantsTOR Serine-Threonine KinasesAMPKCuprizonemTORMultiple sclerosisNrf2

Identifiers

PMID32048246
OpenAlexW3007770903

What Socratic 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 Socratic graph.