Evidence map›Paper›PMID 26329786›Full record

ArticleScientific reports2015

18β-glycyrrhetinic acid suppresses experimental autoimmune encephalomyelitis through inhibition of microglia activation and promotion of remyelination.

Jieru Zhou, Wei Cai, Min Jin, Jingwei Xu, Yanan Wang, Yichuan Xiao, Li Hao, Bei Wang, Yanyun Zhang, Jie Han and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
7.2field-weighted citation impact, top 3% 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

22 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Protective effect of 18β-glycyrrhetinic acid against HExperimental and therapeutic medicine · 2021
    Article
  10. Article
  11. Review
  12. Review
  13. The "Treatise on the spleen and stomach" (Journal of traditional and complementary medicine · 2020
    Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. Article
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 5 institutions in 1 country.

Jieru ZhouDepartment of Rheumatology, East Hospital, Tongji University School of Medicine, Shanghai, China.
Wei CaiDepartment of Infectious Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Min JinMedical College of Soochow University, Suzhou, Jiangsu, China.
Jingwei XuKey Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences and Shanghai Jiao Tong University School of Medicine (SJTUSM), and Shanghai Institute of Immunology, Institutes of Medical Sciences, SJTUSM, Shanghai, China.
Yanan WangKey Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences and Shanghai Jiao Tong University School of Medicine (SJTUSM), and Shanghai Institute of Immunology, Institutes of Medical Sciences, SJTUSM, Shanghai, China.
Yichuan XiaoKey Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences and Shanghai Jiao Tong University School of Medicine (SJTUSM), and Shanghai Institute of Immunology, Institutes of Medical Sciences, SJTUSM, Shanghai, China.
Li HaoClinical Laboratory, the First Affiliated Hospital of Anhui Medical University, Hefei, China.
Bei WangKey Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences and Shanghai Jiao Tong University School of Medicine (SJTUSM), and Shanghai Institute of Immunology, Institutes of Medical Sciences, SJTUSM, Shanghai, China.
Yanyun ZhangKey Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences and Shanghai Jiao Tong University School of Medicine (SJTUSM), and Shanghai Institute of Immunology, Institutes of Medical Sciences, SJTUSM, Shanghai, China.
Jie HanDepartment of Rheumatology, East Hospital, Tongji University School of Medicine, Shanghai, China.
Rui HuangMedical College of Soochow University, Suzhou, Jiangsu, China.
Shanghai Jiao Tong University · CNShanghai East Hospital · CNAnhui Medical University · CNRuijin Hospital · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microglia are intrinsic immune cells in the central nervous system (CNS). The under controlled microglia activation plays important roles in inflammatory demyelination diseases, such as multiple sclerosis (MS). However, the means to modulate microglia activation as a therapeutic modality and the underlying mechanisms remain elusive. Here we show that administration of 18β-glycyrrhetinic acid (GRA), by using both preventive and therapeutic treatment protocols, significantly suppresses disease severity of experimental autoimmune encephalomyelitis (EAE) in C57BL/6 mice. The treatment effect of GRA on EAE is attributed to its regulatory effect on microglia. GRA-modulated microglia significantly decreased pro-inflammatory profile in the CNS through suppression of MAPK signal pathway. The ameliorated CNS pro-inflammatory profile prevented the recruitment of encephalitogenic T cells into the CNS, which alleviated inflammation-induced demyelination. In addition, GRA treatment promoted remyelination in the CNS of EAE mice. The induced remyelination can be mediated by the overcome of inflammation-induced blockade of brain-derived neurotrophic factor expression in microglia, as well as enhancing oligodendrocyte precursor cell proliferation. Collectively, our results demonstrate that GRA-modulated microglia suppresses EAE through inhibiting microglia activation-mediated CNS inflammation, and promoting neuroprotective effect of microglia, which represents a potential therapeutic strategy for MS and maybe other neuroinflammatory diseases associated with microglia activation.

Indexed as

AnimalsAstrocytesBrain-Derived Neurotrophic FactorCentral Nervous SystemChemokinesEncephalomyelitis, Autoimmune, ExperimentalGlycyrrhetinic AcidInflammationMAP Kinase Signaling SystemMice, Inbred C57BLMicrogliaMyelin SheathT-Lymphocytes18alpha-glycyrrhetinic acidBrain-Derived Neurotrophic FactorChemokinesGlycyrrhetinic Acid

Identifiers

PMID26329786
PMCPMC4557075
OpenAlexW1229963475

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.