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Open AccessJournal ArticleDOI

Inhibitory effects of anti-inflammatory drugs on type II collagen induced arthritis in rats.

K Yamaki, +2 more
- 01 Jul 1987 - 
- Vol. 46, Iss: 7, pp 543-548
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TLDR
It is indicated that non-steroidal anti-inflammatory drugs having inhibitory action on cyclo-oxygenase are useful antiarthritic drugs without causing the rebound phenomenon, an untoward side effect after withdrawal of steroidal anti- inflammatory drugs.
Abstract
The effects of steroidal and non-steroidal anti-inflammatory drugs on the established lesion of type II collagen induced arthritis in rats were evaluated by measuring the hind paw oedema and anti-type II collagen antibody titre. Dexamethasone, a steroidal anti-inflammatory drug, reduced the anti-type II collagen antibody titre and markedly suppressed the established lesion of type II collagen induced arthritis in rats. A rebound of the arthritis, i.e., a rapid recovery of the hind paw swelling took place after withdrawal of the treatment with steroidal anti-inflammatory drugs, including dexamethasone, prednisolone, and hydrocortisone. On the other hand, indomethacin, benoxaprofen, piroxicam, and tiflamizole, which are cyclo-oxygenase inhibitors in prostaglandin synthesis, had no effect on anti-type II collagen antibody titre, but suppressed the established lesion of the arthritis without causing an apparent rebound of the arthritis after withdrawal of the drug treatment. These results suggest that the level of anti-type II collagen antibodies has no relation to the intensity of hind paw swelling in the established lesion of the arthritis, though the antibodies contribute to the incidence of the arthritis. It also indicates that non-steroidal anti-inflammatory drugs having inhibitory action on cyclo-oxygenase are useful antiarthritic drugs without causing the rebound phenomenon, an untoward side effect after withdrawal of steroidal anti-inflammatory drugs.

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Resolution‐associated molecular patterns (RAMP): RAMParts defending immunological homeostasis?

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Old and new therapeutics for Rheumatoid Arthritis: in vivo models and drug development.

TL;DR: A number of existing rodent models for Rheumatoid Arthritis are reviewed in the context of how these models have been utilized for developing established therapy in Rhe autoimmune diseases and, furthermore, the present use of animal models for studies of novel drug candidates.
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Interleukin 1 mediated acceleration of type II collagen-induced arthritis: effects of anti-inflammatory or anti-arthritic drugs.

TL;DR: Because of the shorter latent period required for the development of arthritis in theIL-1 treated animals, the IL-1 accelerated CIA model in both mice and rats may be useful for screening anti-inflammatory or anti-arthritic compounds.
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Immunopharmacological studies on collagen-induced arthritis in dark Agouti (DA) rats.

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References
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Journal ArticleDOI

Autoimmunity to type II collagen an experimental model of arthritis.

TL;DR: Since homologous type II collagen emulsified in oil without bacterial preparations regularly causes the disease, this new animal model of arthritis represents a unique example of experimentally-inducible autoimmunity to a tissue component.
Journal ArticleDOI

Production of collagenase and prostaglandins by isolated adherent rheumatoid synovial cells

TL;DR: In this article, the authors studied cells dispersed with proteolytic enzymes from rheumatoid arthritic synovectomy specimens to determine the cell type(s) responsible for joint destruction, and found that 10-50% of these cells adhered to culture dishes within 24 hours and were of two main types: small, round cells and larger, stellate cells.
Journal ArticleDOI

Prostaglandin-stimulated bone resorption by rheumatoid synovia. A possible mechanism for bone destruction in rheumatoid arthritis.

TL;DR: It is concluded that the bone resorption-stimulating activity produced by rheumatoid synovia in culture is PGE2, itself a potent osteolytic factor.
Journal ArticleDOI

The pharmacology of benoxaprofen (2‐[4‐chlorophenyl]‐α‐methyl‐5‐benzoxazole acetic acid), LRCL 3794, a new compound with anti‐inflammatory activity apparently unrelated to inhibition of prostaglandin synthesis

TL;DR: Benoxaprofen has analgesic activity in tests where pain is accompanied by inflammation but not in other experimental models of pain, and its low ulcerogenic potential in animal models may be related to its relative inability to inhibit PG synthetase.
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