Methotrexate as a preferential cyclooxygenase 2 inhibitor in whole blood of patients with rheumatoid arthritis
Rheumatology, ISSN: 1462-0324, Vol: 39, Issue: 5, Page: 533-536
2000
- 47Citations
- 17Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations47
- Citation Indexes46
- 46
- CrossRef34
- Patent Family Citations1
- Patent Families1
- Captures17
- Readers17
- 17
Article Description
Objective. To investigate the regulation of whole-blood cyclooxygenase-1 and -2 (COX-2 and COX-1) activities by methotrexate (MTX) in rheumatoid arthritis (RA) patients. Methods. Whole blood was withdrawn from nine healthy volunteers, 12 RA patients treated with MTX (RA/MTX) and six RA patients treated with chloroquine (RA/CQ). COX-1 activity was quantified as platelet thromboxane B production in unstimulated blood and COX-2 activity was measured as prostaglandin E (PGE) production in whole blood stimulated with LPS. Thromboxane B and PGE were measured by radioimmunoassay. We studied the drug effect in vitro by direct incubation of MTX with blood obtained from normal donors. Ex vivo assays were performed with blood collected from RA/MTX and RA/CQ patients. The influence of serum factors on enzyme activities was analysed in blood collected from normal donors and incubated with RA/MTX, autologous or heterologous serum. Results. In vitro assays showed no direct action of MTX on the activity of either enzyme. Assays performed with blood from RA/MTX patients showed preferential inhibition of COX-2 activity (PGE = 10.11 ± 2.42 ng/ml) when compared with blood of normal donors (PGE = 37.7 ± 4.36 ng/ml; P = 0.001). Inhibition of COX-2 activity was also observed when blood of normal donors was co-incubated with RA/MTX serum. Conclusion. Our results clearly show that the anti-inflammatory action of low-dose MTX is partly mediated by a serum factor induced by MTX or a MTX metabolite that preferentially inhibits the activity of COX-2.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0034119415&origin=inward; http://dx.doi.org/10.1093/rheumatology/39.5.533; http://www.ncbi.nlm.nih.gov/pubmed/10852985; https://academic.oup.com/rheumatology/article-lookup/doi/10.1093/rheumatology/39.5.533; https://dx.doi.org/10.1093/rheumatology/39.5.533; https://academic.oup.com/rheumatology/article-abstract/39/5/533/1784111?redirectedFrom=fulltext
Oxford University Press (OUP)
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