Evidence map›Paper›PMID 26616302›Full record

ArticleScientific reports2015

Therapeutic effect of baicalin on experimental autoimmune encephalomyelitis is mediated by SOCS3 regulatory pathway.

Yuan Zhang, Xing Li, Bogoljub Ciric, Cun-Gen Ma, Bruno Gran, Abdolmohamad Rostami, Guang-Xian Zhang

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 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
5.9field-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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Pooled it
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  15. Drug Candidates for Autoimmune Diseases.Pharmaceuticals (Basel, Switzerland) · 2022
    Review
  16. Baicalin Promotes CNS Remyelination via PPARγ Signal Pathway.Neurology(R) neuroimmunology & neuroinflammation · 2022
    Article
  17. Article
  18. 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

7 authors at 3 institutions in 3 countries.

Yuan ZhangDepartment of Neurology, Thomas Jefferson University, Philadelphia, PA, USA.
Xing LiDepartment of Neurology, Thomas Jefferson University, Philadelphia, PA, USA.
Bogoljub CiricDepartment of Neurology, Thomas Jefferson University, Philadelphia, PA, USA.
Cun-Gen MaInstitute of Brain Science, Department of Neurology, Shanxi Datong University Medical School, Datong, China.
Bruno GranClinical Neurology Research Group, Division of Clinical Neuroscience, University of Nottingham School of Medicine, UK.
Abdolmohamad RostamiDepartment of Neurology, Thomas Jefferson University, Philadelphia, PA, USA.
Guang-Xian ZhangDepartment of Neurology, Thomas Jefferson University, Philadelphia, PA, USA.
Thomas Jefferson University · USShanxi Datong University · CNUniversity of Nottingham · GB

Funding

NSCs produce a triply effective cocktail in the CNS for MS/EAE therapyR01NS075260 · NINDS · THOMAS JEFFERSON UNIVERSITY · PI ZHANG, GUANG-XIAN · 2012 to 2016
$1.5M
NINDS NIH HHS R01 NS075260
6 · The paper itself

Abstract

Natural compounds derived from medicinal plants have long been considered a rich source of novel therapeutic agents. Baicalin (Ba) is a bioactive flavonoid compound derived from the root of Scutellaria baicalensis, an herb widely used in traditional medicine for the treatment of various inflammatory diseases. In this study, we investigate the effects and mechanism of action of Ba in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). Ba treatment effectively ameliorated clinical disease severity in myelin oligodendrocyte glycoprotein (MOG)35-55 peptide-induced EAE, and reduced inflammation and demyelination of the central nervous system (CNS). Ba reduced infiltration of immune cells into the CNS, inhibited expression of proinflammatory molecules and chemokines, and prevented Th1 and Th17 cell differentiation via STAT/NFκB signaling pathways. Further, we showed that SOCS3 induction is essential to the effects of Ba, given that the inhibitory effect of Ba on pathogenic Th17 responses was largely abolished when SOCS3 signaling was knocked down. Taken together, our findings demonstrate that Ba has significant potential as a novel anti-inflammatory agent for therapy of autoimmune diseases such as MS.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalCell DifferentiationCytokinesDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalFemaleFlavonoidsInflammation MediatorsLymphocyte ActivationMiceMultiple SclerosisNF-kappa BSignal TransductionSTAT Transcription FactorsSuppressor of Cytokine Signaling 3 ProteinAnti-Inflammatory Agents, Non-SteroidalbaicalinCytokinesFlavonoidsInflammation MediatorsNF-kappa BSocs3 protein, mouseSTAT Transcription FactorsSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling Proteins

Identifiers

PMID26616302
PMCPMC4663791
OpenAlexW2420824370

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.