ArticleAnnals of the rheumatic diseases2004
Divergent roles of nitrergic and prostanoid pathways in chronic joint inflammation.
Article in Annals of the rheumatic diseases, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 17 citations in OpenAlex.
- Electroporation-enhanced transdermal diclofenac sodium delivery into the knee joint in a rat model of acute arthritis.Drug design, development and therapy · 2018Article
- Interdicting protease-activated receptor-2-driven inflammation with cell-penetrating pepducins.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Can L(+)-lactate be used as a marker of experimentally induced inflammation in rats?Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2010Article
- Oral phosphatidylcholine pretreatment alleviates the signs of experimental rheumatoid arthritis.Arthritis research & therapy · 2009Article
- Quantitative assessment of synovial vascularity using contrast-enhanced power Doppler ultrasonography: correlation with histologic findings and mr imaging findings in arthritic rabbit knee model.Korean journal of radiologyArticle
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Authors and funding
4 authors at 2 institutions in 1 country.
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Abstract
backgroundNitrergic and prostanoid pathways have both been implicated in inflammatory processes.
objectiveTo investigate their respective contributions in a rat model of chronic arthritis.
methodsMale Wistar rats (n = 4-6/group) received either an intra-articular injection of 2% carrageenan/4% kaolin (C/K) or intra- and periarticular injections of Freund's complete adjuvant (FCA; 10 mg/ml M tuberculosis). Joint diameter, urinary nitric oxide metabolites (NO(x)), and prostaglandin E(2) (PGE(2)) levels were measured as indices of the inflammatory process. A prophylactic and therapeutic (day 5) dose ranging study of an inducible nitric oxide synthase inhibitor, L-N-(1-iminoethyl)-lysine (L-NIL), and a cyclo-oxygenase-2 (COX-2) inhibitor, SC-236, was performed with the drugs given subcutaneously. Submaximal doses were identified and used for combination studies. Appropriate vehicle controls were included.
resultsL-NIL and SC-236 dose dependently inhibited C/K induced acute joint swelling, the magnitude being greatest when they were given in combination. Both prophylactic and therapeutic administration of SC-236 in the FCA induced model of chronic arthritis produced a dose dependent reduction in all the measures assessed. However, although L-NIL demonstrated similar dose dependent inhibition of urinary NO(x) and PGE(2) levels, joint swelling was significantly exacerbated in this model. Co-administration of the inhibitors nullified the benefits of SC-236.
conclusionWhereas COX-2 derived prostaglandins are proinflammatory in both acute and chronic joint inflammation, NO seems to have divergent roles, being anti-inflammatory in chronic and proinflammatory in acute joint inflammation.
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