Evidence map›Paper›PMID 22854193›Full record

ArticleBioorganic & medicinal chemistry2012

Suppression of autoimmune arthritis by Celastrus-derived Celastrol through modulation of pro-inflammatory chemokines.

Shivaprasad H Venkatesha, Brian Astry, Siddaraju M Nanjundaiah, Hua Yu, Kamal D Moudgil

Abstract read
In one paragraph

Article in Bioorganic & medicinal chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
15.7field-weighted citation impact, top 1% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Chondro-protective effects of celastrol on osteoarthritis through autophagy activation and NF-κB signaling pathway inhibition.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020
    Article
  8. Clinical Practice Guideline forFrontiers in pharmacology · 2020
    Article
  9. Article
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  11. Article
  12. Article
  13. Review
  14. Article
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  16. Review
  17. Article
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  20. Celastrol Ameliorates EAE Induction by Suppressing Pathogenic T Cell Responses in the Peripheral and Central Nervous Systems.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2015
    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

5 authors at 1 institution in 1 country.

Shivaprasad H VenkateshaDepartment of Microbiology and Immunology, University of Maryland School of Medicine, 685 W. Baltimore Street, HSF-1, Suite-380, Baltimore, MD 21201, USA.
Brian Astry
Siddaraju M Nanjundaiah
Hua Yu
Kamal D Moudgil
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
NCCIH NIH HHS R01 AT004321NCCIH NIH HHS R01AT004321
6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation of the synovial joints, deformities, and disability. The prolonged use of conventional anti-inflammatory drugs is associated with severe adverse effects. Therefore, there is an urgent need for safer and less expensive therapeutic products. Celastrol is a bioactive component of Celastrus, a traditional Chinese medicine, and it possesses anti-arthritic activity. However, the mechanism of action of Celastrol remains to be fully defined. In this study based on the rat adjuvant-induced arthritis (AA) model of RA, we examined the effect of Celastrol on two of the key mediators of arthritic inflammation, namely chemokines and their receptors, and related pro-inflammatory cytokines. We treated arthritic Lewis rats with Celastrol (200μg/rat) or its vehicle by daily intraperitoneal (ip) injection beginning at the onset of AA. At the peak phase of AA, the sera, the draining lymph node cells, spleen adherent cells, and synovial-infiltrating cells of these rats were harvested and tested. Celastrol-treated rats showed a significant reduction in the levels of chemokines (RANTES, MCP-1, MIP-1α, and GRO/KC) as well as cytokines (TNF-α and IL-1β) that induce them, compared to the vehicle-treated rats. However, Celastrol did not have much effect on cellular expression of chemokine receptors except for an increase in CCR1. Further, Celastrol inhibited the migration of spleen adherent cells in vitro. Thus, Celastrol-induced suppression of various chemokines that mediate cellular infiltration into the joints might contribute to its anti-arthritic activity. Our results suggest that Celastrol might offer a promising alternative/adjunct treatment for RA.

Indexed as

AnimalsAnti-Inflammatory AgentsArthritis, RheumatoidCelastrusCell MovementChemokinesCytokinesDisease Models, AnimalFlow CytometryMalePentacyclic TriterpenesRatsRats, Inbred LewReceptors, ChemokineSpleenTriterpenesAnti-Inflammatory AgentscelastrolChemokinesCytokinesPentacyclic TriterpenesReceptors, ChemokineTriterpenes

Identifiers

PMID22854193
PMCPMC3449088
OpenAlexW2009731763

What OpenQuestion holds

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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.