Humes J L, Sadowski S, Galavage M, Goldenberg M, Subers E, Kuehl F A, Bonney R J
Biochem Pharmacol. 1983 Aug 1;32(15):2319-22. doi: 10.1016/0006-2952(83)90179-x.
Resident mouse peritoneal macrophages, exposed to zymosan, synthesized and released products of both the cyclooxygenase and lipoxygenase pathways. The effects of various non-steroidal antiinflammatory agents were evaluated for their abilities to inhibit zymosan-stimulated prostaglandin E2 (PGE2) and leukotriene C4 (LTC4) synthesis. The order of potencies to inhibit PGE2 synthesis and release was: indomethacin greater than or equal to sulindac sulfide greater than ibuprofen greater than or equal to aspirin greater than 3-amino-1-[3-(trifluoromethyl)-phenyl]-2-pyrazoline (BW755C) greater than benoxaprofen greater than or equal to nordihydroguaiaretic acid (NDGA) greater than 5,8,11-eicosatriynoic acid (ETYA). BW755C and ETYA also inhibited zymosan-stimulated LTC4 production. None of the compounds tested showed selective inhibition of lipoxygenase products.
暴露于酵母聚糖的小鼠腹腔巨噬细胞能合成并释放环氧化酶和脂氧合酶途径的产物。评估了各种非甾体抗炎药抑制酵母聚糖刺激的前列腺素E2(PGE2)和白三烯C4(LTC4)合成的能力。抑制PGE2合成和释放的效力顺序为:吲哚美辛≥舒林酸硫化物>布洛芬≥阿司匹林>3-氨基-1-[3-(三氟甲基)苯基]-2-吡唑啉(BW755C)>苯恶洛芬≥去甲二氢愈创木酸(NDGA)>5,8,11-二十碳三烯酸(ETYA)。BW755C和ETYA也抑制酵母聚糖刺激的LTC4产生。所测试的化合物均未显示对脂氧合酶产物的选择性抑制。