Evidence map›Paper›PMID 18536737›Full record

ArticleBritish journal of pharmacology2008

Effect of chondroitin sulphate in a rabbit model of atherosclerosis aggravated by chronic arthritis.

G Herrero-Beaumont, M E Marcos, O Sánchez-Pernaute, R Granados, L Ortega, E Montell, J Vergés, J Egido, R Largo

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

23 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Fluid shear stress induces upregulation of COX-2 and PGIAmerican journal of physiology. Heart and circulatory physiology · 2017
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Use of glucosamine and chondroitin in relation to mortality.European journal of epidemiology · 2012
    Article
  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

9 authors at 4 institutions in 1 country.

G Herrero-BeaumontJoint and Bone Research Unit and Vascular Research Laboratory, Fundación Jiménez Díaz, Universidad Autónoma, Madrid, Spain.
M E Marcos
O Sánchez-Pernaute
R Granados
L Ortega
E Montell
J Vergés
J Egido
R Largo
Hospital Universitario Fundación Jiménez Díaz · ESBioibérica (Spain) · ESHospital Clínico San Carlos · ESHospital Universitario de Getafe · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeAmong the agents employed to manage osteoarthritis, chondroitin sulphate (CS) is a natural glycosaminoglycan with an anti-inflammatory effect on joint cells. CS might also influence the inflammatory component of atherosclerosis. Our aim was to examine the effect of CS administration on vascular injury and on markers of systemic inflammation in a rabbit model of atherosclerosis aggravated by systemic inflammation provoked by chronic antigen-induced arthritis. EXPERIMENTAL APPROACH: Atherosclerosis was induced in rabbits by maintaining them on a hyperlipidaemic diet after producing an endothelial lesion in the femoral arteries. Simultaneously, chronic arthritis was induced in these animals by repeated intraarticular injections of ovalbumin in previously immunized rabbits. A group of these rabbits were treated prophylactically with CS (100 mg kg(-1)day(-1)) and when the animals were killed, serum and peripheral blood mononuclear cells (PBMC) were isolated. Furthermore, femoral arteries and thoracic aorta were used for gene expression studies and histological examination. KEY

resultsCS administration reduced the concentration of the proinflammatory molecules C-reactive protein and IL-6 in serum. Likewise, CS inhibited the expression of CCL2/monocyte chemoattractant protein (MCP)-1 and cyclooxygenase (COX)-2 in PBMC, and reduced the nuclear translocation of nuclear factor-kappaB. In the femoral lesion, CS also diminished the expression of CCL2 and COX-2, as well as the ratio of the intima/media thickness. Moreover, CS decreased the percentage of rabbits with atherosclerosis and chronic arthritis that developed vascular lesions in the aorta. CONCLUSIONS AND IMPLICATIONS: These findings suggest that CS treatment may to some extent impede the progression of atherosclerosis.

Indexed as

AnimalsAnti-Inflammatory AgentsAortaArthritis, ExperimentalAtherosclerosisChemokine CCL2Chondroitin SulfatesC-Reactive ProteinCyclooxygenase 2Disease Models, AnimalDisease ProgressionGene Expression RegulationInflammationInterleukin-6MaleNF-kappa BAnti-Inflammatory AgentsChemokine CCL2Chondroitin SulfatesC-Reactive ProteinCyclooxygenase 2Interleukin-6NF-kappa B

Identifiers

PMID18536737
PMCPMC2439856
OpenAlexW1900801758

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.