Effects of anti-inflammatory drugs on cartilage recovery from catabolin-induced degradation.
Effects of aspirin (200 micrograms/ml), hydrocortisone (10 micrograms/ml), sodium aurothiomalate (100 micrograms/ml), and indomethacin (10 micrograms/ml) on recovery of cartilage from interleukin 1 or catabolin-induced degradation were examined in this initial in vitro study. The experimental protocol involved a "degradative phase" of eight days during which cartilage plugs were incubated in the presence or absence of spent human rheumatoid synovial culture media. A "recovery" period of six days followed during which the effects of the aforementioned drugs on treated cartilage were analyzed. Incorporation of [35S]sulfate and [3H]proline precursors, and total contents of hydroxyproline and glycosaminoglycan in cartilage were determined two, four, and six days after insult. Aspirin treatment caused a rise in total proteoglycan content over degraded controls (p less than 0.002), however, this increase was not associated with increased [35S]sulfate incorporation into glycosaminoglycans. Hydrocortisone resulted in a delayed rise in proteoglycan content concommitant with increased [35S]sulfate uptake, whereas sodium aurothiomalate treatment was without effect on proteoglycans. Indomethacin treatment was associated with an increased release of newly synthesized macromolecules by cartilage into the media (p less than 0.01). These results suggest that common anti-inflammatory drugs may exhibit distinctly different effects on the in vitro synthesis and retention of proteoglycans by cartilage explants previously exposed to a degradative phase. Further work is necessary to assess the influence of drug concentration in this experimental system.
D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001241:Aspirin / Q000494:pharmacology*; D002356:Cartilage / Q000187:drug effects* / Q000378:metabolism; D005109:Extracellular Matrix / Q000378:metabolism; D006052:Gold Sodium Thiomalate / Q000494:pharmacology*; D006801:Humans; D006854:Hydrocortisone / Q000494:pharmacology*; D006909:Hydroxyproline / Q000096:biosynthesis; D007213:Indomethacin / Q000494:pharmacology*; D007375:Interleukin-1 / Q000633:toxicity*; D053583:Interleukin-1beta; D011509:Proteoglycans / Q000096:biosynthesis
D000893:Anti-Inflammatory Agents; D007375:Interleukin-1; D053583:Interleukin-1beta; D011509:Proteoglycans; D006052:Gold Sodium Thiomalate; D001241:Aspirin; D006909:Hydroxyproline; D006854:Hydrocortisone; D007213:Indomethacin