Klaushofer K, Hoffmann O, Czerwenka E, Leis H J, Gleispach H, Koller K, Peterlik M
Ludwig Boltzmann Research Unit for Clinical and Experimental Osteology, Hanusch Hospital, Vienna, Austria.
J Rheumatol. 1988 Mar;15(3):486-91.
The biopotency of various nonsteroidal antiinflammatory drugs (NSAID) in inhibiting prostaglandin (PG) mediated bone resorption was evaluated in a neonatal mouse calvaria organ culture system. Thrombin stimulated formation of the osteolytic PG, PGE2 and PGI2 (measured as 6-keto-PGF1 alpha) and the concomitant stimulation of calcium release from cultured bone were inhibited by diclofenac much greater than indomethacin much greater than flurbiprofen greater than piroxicam greater than acemetacin much greater than acetylsalicylic acid. The relative potencies of the NSAID on PG synthesis in bone differs from that observed previously in other model systems.
在新生小鼠颅骨器官培养系统中评估了各种非甾体抗炎药（NSAID）抑制前列腺素（PG）介导的骨吸收的生物效能。凝血酶刺激溶骨性PG、PGE2和PGI2（以6-酮-PGF1α衡量）的形成以及培养骨中钙释放的伴随刺激，双氯芬酸对其的抑制作用远大于吲哚美辛，远大于氟比洛芬，大于吡罗昔康，远大于阿西美辛，远大于乙酰水杨酸。NSAID对骨中PG合成的相对效能与先前在其他模型系统中观察到的不同。
