Shirota H, Goto M, Hashida R, Yamatsu I, Katayama K
Eisai Research Laboratories, Eisai Co., Ltd., Ibaraki, Japan.
Agents Actions. 1989 Jun;27(3-4):322-4. doi: 10.1007/BF01972811.
Effects of E-5110, a novel non-steroidal antiinflammatory drug, on interleukin-1 (IL-1) generation from human monocytes were studied in vitro. E-5110 reduced the amounts of extra- and intracellular IL-1 activity induced by lipopolysaccharide (LPS, 1 micrograms/ml) in a dose-dependent manner (1-10 microM). E-5110 also inhibited the IL-1 generation induced by antigen-antibody complexes, opsonized zymosan and silica particles. It was suggested that the inhibition of IL-1 generation by E-5110 was independent of the inhibitory effects on arachidonate cyclooxygenase and/or lipoxygenase because indomethacin, piroxicam, BW755C and AA861 had no effects on IL-1 generation. Hydrocortisone (IC50:0.084 microM), aurothioglucose (11.5 microM) and lobenzarit (75.0 microM), which are clinically effective antirheumatic drugs, also inhibited IL-1 generation, like E-5110 (1.21 microM). It is expected that E-5110 will be superior to classical non-steroidal antiinflammatory drugs in medical treatment of rheumatoid arthritis.
研究了新型非甾体抗炎药E - 5110对人单核细胞白细胞介素 - 1（IL - 1）生成的体外作用。E - 5110以剂量依赖性方式（1 - 10 microM）降低了脂多糖（LPS，1微克/毫升）诱导的细胞外和细胞内IL - 1活性水平。E - 5110还抑制了抗原 - 抗体复合物、调理酵母聚糖和二氧化硅颗粒诱导的IL - 1生成。提示E - 5110对IL - 1生成的抑制作用独立于对花生四烯酸环氧化酶和/或脂氧合酶的抑制作用，因为吲哚美辛、吡罗昔康、BW755C和AA861对IL - 1生成无影响。临床有效的抗风湿药物氢化可的松（IC50：0.084 microM）、金硫葡萄糖（11.5 microM）和苯扎利特（75.0 microM）也像E - 5110（1.21 microM）一样抑制IL - 1生成。预计E - 5110在类风湿性关节炎的医学治疗中优于经典非甾体抗炎药。
