Benslay D N, Nickander R
Agents Actions. 1982 Jul;12(3):313-9. doi: 10.1007/BF01965396.
Benoxaprofen, a new nonsteroidal anti-inflammatory agent recently marketed as an an antirheumatic drug, has been reported to suppress leucocyte migration into inflammatory sites, possibly by its reported inhibition of leukotriene synthesis. Benoxaprofen is also a weak to moderate inhibitor of prostaglandin synthesis. The effect of benoxaprofen was examined on adjuvant-induced arthritis in rats by radiographic assessment of bone damage. The effect of benoxaprofen was compared to other nonsteroidal anti-inflammatory agents, considered to act primarily by the inhibition of synthesis and/or release of prostaglandins. Drugs were administered from the 15th to the 30th day after induction of the adjuvant disease ('established adjuvant'). Radiographs of adjuvant rats showed extensive bone damage that was markedly suppressed by 30-40 mg/kg of benoxaprofen. Benoxaprofen exerted a dose-related inhibition of bone damage. There was less suppression of bone damage by comparable doses of phenylbutazone, oxyphenbutazone, ibuprofen, fenbufen, naproxen, tolectin and sulindac. Indomethacin, piroxicam and flurbiprofen were nearly as effective but only in doses that produced adverse effects or death in rats. Benoxaprofen may modify the progression of the experimental arthritic disease through a suppression of leucocyte migration.
苯恶洛芬是一种最近作为抗风湿药物上市的新型非甾体抗炎药,据报道它能抑制白细胞向炎症部位迁移,可能是通过其对白三烯合成的抑制作用。苯恶洛芬也是前列腺素合成的弱至中度抑制剂。通过对骨损伤的影像学评估,研究了苯恶洛芬对佐剂诱导的大鼠关节炎的影响。将苯恶洛芬的作用与其他非甾体抗炎药进行了比较,这些药物被认为主要通过抑制前列腺素的合成和/或释放起作用。在佐剂性疾病诱导后第15天至第30天(“已确立的佐剂性疾病”)给药。佐剂性大鼠的X线片显示广泛的骨损伤,30 - 40mg/kg的苯恶洛芬可显著抑制这种损伤。苯恶洛芬对骨损伤的抑制作用呈剂量相关性。同等剂量的保泰松、羟基保泰松、布洛芬、芬布芬、萘普生、托美丁和舒林酸对骨损伤的抑制作用较小。吲哚美辛、吡罗昔康和氟比洛芬的效果几乎相同,但仅在能导致大鼠出现不良反应或死亡的剂量下有效。苯恶洛芬可能通过抑制白细胞迁移来改变实验性关节炎疾病的进程。