Evidence map›Paper›PMID 30820608›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2019

Celastrol suppresses experimental autoimmune encephalomyelitis via MAPK/SGK1-regulated mediators of autoimmune pathology.

Shivaprasad H Venkatesha, Kamal D Moudgil

Open access · greenAbstract read
In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
5.3field-weighted citation impact, top 5% 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

16 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. The role of celastrol in inflammation and diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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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

2 authors at 1 institution in 1 country.

Shivaprasad H VenkateshaDepartment of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD, 21201, USA.
Kamal D MoudgilDepartment of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD, 21201, USA. kmoudgil@som.umaryland.edu.
University of Maryland, Baltimore · US

Funding

Immune Modulation of Autoimmunity by Herbal ProductsR01AT004321 · NCCIH · UNIVERSITY OF MARYLAND BALTIMORE · PI MOUDGIL, KAMAL D · 2009 to 2012
$1.5M
Identification of CNS-homing peptides for therapeutic use in multiple sclerosisR21NS082918 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI MOUDGIL, KAMAL D · 2013 to 2014
$420k
Anti-arthritic activity and therapeutic use of novel joint-homing peptidesI01BX002424 · VA · BALTIMORE VA MEDICAL CENTER · PI MOUDGIL, KAMAL D · 2015 to 2018
–
BLRD VA I01 BX002424National Institutes of Health, Bethesda, USA 1R21NS082918National Institutes of Health, Bethesda, USA R01 AT 004321NCCIH NIH HHS R01 AT004321NINDS NIH HHS R21 NS082918U.S. Department of Veterans Affairs I01 BX002424
6 · The paper itself

Abstract

OBJECTIVE AND

designMultiple sclerosis (MS) is a debilitating autoimmune disease involving immune dysregulation of the pathogenic T helper 17 (Th17) versus protective T regulatory (Treg) cell subsets, besides other cellular aberrations. Studies on the mechanisms underlying these changes have unraveled the involvement of mitogen-activated protein kinase (MAPK) pathway in the disease process. We describe here a gene expression- and bioinformatics-based study showing that celastrol, a natural triterpenoid, acting via MAPK pathway regulates the downstream genes encoding serum/glucocorticoid regulated kinase 1 (SGK1), which plays a vital role in Th17/Treg differentiation, and brain-derived neurotrophic factor (BDNF), which is a neurotrophic factor, thereby offering protection against experimental autoimmune encephalomyelitis (EAE) in mice.

methodsWe first tested the gene expression profile of splenocytes of EAE mice in response to the disease-related antigen, myelin oligodendrocyte glycoprotein (MOG), and then examined the effect of celastrol on that profile.

resultsInterestingly, celastrol reversed the expression of many MOG-induced genes involved in inflammation and immune pathology. The MAPK pathway involving p38MAPK and ERK was identified as one of the mediators of celastrol action. It involved suppression of SGK1 but upregulation of BDNF, which then contributed to protection against EAE.

conclusionOur results not only provide novel insights into disease pathogenesis, but also offer promising therapeutic targets for MS.

Indexed as

Anti-Inflammatory AgentsImmunologic FactorsTriterpenesAnimalsBrain-Derived Neurotrophic FactorCytokinesEncephalomyelitis, Autoimmune, ExperimentalGene Expression RegulationImmediate-Early ProteinsMaleMice, Inbred C57BLMitogen-Activated Protein KinasesMyelin-Oligodendrocyte GlycoproteinPentacyclic TriterpenesProtein Serine-Threonine KinasesSerum-Glucocorticoid Regulated KinasesAnti-Inflammatory AgentsBdnf protein, mouseBrain-Derived Neurotrophic FactorcelastrolCytokinesImmediate-Early ProteinsImmunologic FactorsMitogen-Activated Protein KinasesMyelin-Oligodendrocyte GlycoproteinPentacyclic TriterpenesProtein Serine-Threonine KinasesSerum-Glucocorticoid Regulated KinasesTriterpenesAutoimmune diseasesBDNFCelastrolEAEMultiple sclerosisP38 MAPKSGK1Th17/Treg balance

Identifiers

PMID30820608
PMCPMC6517245
OpenAlexW2915212160

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.