Brandt K D, Albrecht M E, Kalasinski L A
Rheumatology Division, Indiana University School of Medicine, Indianapolis 46202-5103.
J Clin Pharmacol. 1990 Sep;30(9):808-14. doi: 10.1002/j.1552-4604.1990.tb01878.x.
The effects of tiaprofenic acid (TPA), a nonsteroidal antiinflammatory drug with high potency as a cyclooxygenase inhibitor, on the metabolism of normal and degenerating articular cartilage were examined. When present in the culture medium in clinically relevant concentrations encompassing those achieved in synovial fluid of patients treated with the drug, TPA had no significant effects on net proteoglycan synthesis in organ cultures of normal, osteoarthritic or atrophic canine articular cartilage. When fed to dogs for 8 weeks in a daily dose of 100 mg, TPA had no apparent effect on cartilage water content or uronic acid concentration. The suppression of net cartilage proteoglycan synthesis caused by immobilization was not affected by administration of TPA nor did the drug affect the proportion of newly synthesized glycosaminoglycans recovered from the spent culture medium, suggesting that it did not increase proteoglycan catabolism or affect the integrity of the cartilage matrix.
检测了强效环氧化酶抑制剂非甾体抗炎药替诺昔康(TPA)对正常及退变关节软骨代谢的影响。当在培养基中存在临床相关浓度(涵盖接受该药物治疗患者滑液中所达到的浓度)时,TPA对正常、骨关节炎或萎缩性犬关节软骨器官培养物中的蛋白聚糖净合成无显著影响。当以每日100毫克的剂量喂饲犬8周时,TPA对软骨含水量或糖醛酸浓度无明显影响。固定导致的软骨蛋白聚糖净合成抑制不受TPA给药的影响,该药物也不影响从用过的培养基中回收的新合成糖胺聚糖的比例,这表明它不会增加蛋白聚糖分解代谢或影响软骨基质的完整性。