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Effects of flunixin, tolfenamic acid, R(−) and S(+) ketoprofen on the response of equine synoviocytes to lipopolysaccharide stimulation
Author(s) -
LANDONI M. F.,
FOOT R.,
FREAN S.,
LEES P.
Publication year - 1996
Publication title -
equine veterinary journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.82
H-Index - 87
eISSN - 2042-3306
pISSN - 0425-1644
DOI - 10.1111/j.2042-3306.1996.tb01619.x
Subject(s) - ketoprofen , chemistry , prostaglandin e2 , lipopolysaccharide , pharmacology , stimulation , prostaglandin , endocrinology , biochemistry , medicine , chromatography
Summary The objective of this study was to analyse the effects of 4 nonsteroidal anti‐inflammatory drugs (NSAIDs) on the production of β‐glucuronidase (β‐glu), tumour necrosis factor alpha (TNFα), interleukin‐6 (IL‐6), interleukin‐1 (IL‐1) and prostaglandin E 2 (PGE 2 ) by lipopolysaccharide (LPS)‐stimulated equine synoviocytes. The agents studied were flunixin, tolfenamic acid, S(+)ketoprofen (KTP) and R(‐)ketoprofen. LPS‐induced release of β‐glu from synoviocytes was inhibited in a concentration dependent manner by all 4 compounds, tolfenamic acid being the most potent. Of the 2 KTP enantiomers, S(+)KTP exerted the greatest inhibitory effect. Tolfenamic acid and flunixin increased the production of IL‐6‐like activity by LPS‐stimulated synoviocytes only at the highest concentration studied (1000 μmol/l). Lower concentrations produced no effect on IL‐6. Flunixin, tolfenamic acid and S(+)KTP produced statistically significant and concentration related increases in the release of IL‐1‐like activity by LPS‐stimulated synoviocytes. Prostaglandin E 2 synthesis was markedly inhibited in a concentration dependent manner by the 4 NSAIDs. However, R(‐)KTP was effective only at the highest concentrations investigated (1000 and 100 μmol/l). The present findings are compatible with the possibility that longterm use of NSAIDs in arthropathies, by removing the regulator role of PGE 2 on IL‐1 synthesis, might enhance the pathological process of cartilage degeneration.