Evidence map›Paper›PMID 35976486›Full record

ArticleJournal of molecular neuroscience : MN2022

Ursolic Acid Enhances Myelin Repair in Adult Mice Brains and Stimulates Exhausted Oligodendrocyte Progenitors to Remyelinate.

Fatemeh Honarvar, Vida Hojati, Leila Zare, Nuredin Bakhtiari, Mohammad Javan

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular neuroscience : MN, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Impact of calcitriol and PGDDrug delivery and translational research · 2024
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Remyelination in Multiple Sclerosis: Findings in the Cuprizone Model.International journal of molecular sciences · 2022
    Review
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 1 country.

Fatemeh HonarvarDepartment of Biology, Damghan Branch, Islamic Azad University, Damghan, Iran.
Vida HojatiDepartment of Biology, Damghan Branch, Islamic Azad University, Damghan, Iran.
Leila ZareDepartment of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Nuredin BakhtiariDepartment of Biochemistry, Faculty of Biological Sciences, North Tehran Branch, Islamic Azad University, Tehran, Iran.
Mohammad JavanDepartment of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran. mjavan@modares.ac.ir.
Islamic Azad University, Damghan Branch · IRTarbiat Modares University · IRIslamic Azad University North Tehran Branch · IR

Funding

National Institute for Medical Research Development 971403
6 · The paper itself

Abstract

In multiple sclerosis patients, long-term inflammation makes the oligodendrocyte progenitor cells (OPCs) exhausted; therefore, a new therapy that makes them responsive to insults to participate in remyelination is highly in demand. Here, we investigated the effect of ursolic acid (UA) on myelin repair after mid-term and long-term demyelination periods induced by 6 or 12 weeks of cuprizone treatment followed by 2 weeks of recovery with or without UA. Immunohistochemistry studies and myelin genes expression assessment were used to evaluate the myelination status of mouse corpora callosa and the cellular mechanisms of myelin repair. Results showed that UA significantly promoted recovery from myelin loss after discontinuing 6 or 12 weeks of cuprizone feeding, as measured by luxol fast blue (LFB), fluoroMyelin (FM), anti-myelin basic protein (MBP) staining, and oligodendrocyte progenitor cell counts. It led to reduced inflammation and gliosis as evaluated by glial fibrillary acidic protein (GFAP), Iba1, or other marker gene transcripts. Following long-term demyelination, gliosis and TNF-α were observed as potential players in lesion pathology, which were restored by UA. An increased IL-10 may contribute to UA anti-inflammatory effect and making responsive the exhausted OPCs. UA increased the number of new oligodendrocyte lineage cells and myelination. Our findings indicated that UA can enhance myelin repair after cuprizone challenge through the prevention of gliosis and increasing the newly generated myelin.

Indexed as

Demyelinating DiseasesOligodendrocyte Precursor CellsAnimalsAnti-Inflammatory AgentsCorpus CallosumCuprizoneDisease Models, AnimalGlial Fibrillary Acidic ProteinGliosisInflammationInterleukin-10MiceMice, Inbred C57BLMyelin SheathOligodendrogliaTumor Necrosis Factor-alphaAnti-Inflammatory AgentsCuprizoneGlial Fibrillary Acidic ProteinInterleukin-10Tumor Necrosis Factor-alphaUrsolic AcidAnti-inflammatory effectCuprizone demyelinationMultiple sclerosisMyelin repairUrsolic acid

Identifiers

PMID35976486
OpenAlexW4292324151

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.