Fujisawa H, Nishimura T, Motonaga A, Inoue Y, Inoue K, Suzuka H, Yoshifusa H, Kimura K, Muramatsu M
Research Laboratories, Nippon Shinyaku Co., Ltd., Kyoto, Japan.
Arzneimittelforschung. 1994 Jan;44(1):64-8.
The effect of actarit (MS-932, CAS 18699-02-0), an antirheumatic drug, on type II collagen (CII)-induced arthritis in DBA/1J mice was studied. Mice were immunized twice with bovine CII, actarit being given orally once a day for 35 days after the 1st immunization. Clinical assessment showed that actarit had no effect on the incidence or day of onset of arthritis but that it lowered the arthritis score dose-dependently. Radiography showed that actarit reduced new bone formation in the limbs, and a histopathologic examination showed that it reduced synovitis, erosion of cartilage and bone destruction. Actarit suppressed the delayed-type mouse ear skin reaction to CII but had no effect on the level of serum anti-CII antibodies. These results suggest that actarit inhibits the development of CII-induced arthritis in mice by suppressing delayed-type hypersensitivity to CII.
研究了抗风湿药物阿克他利（MS-932，化学物质登记号18699-02-0）对DBA/1J小鼠Ⅱ型胶原（CII）诱导性关节炎的影响。用牛CII对小鼠进行两次免疫，首次免疫后阿克他利每天口服给药一次，持续35天。临床评估显示，阿克他利对关节炎的发病率或发病日无影响，但能剂量依赖性地降低关节炎评分。X线摄影显示，阿克他利减少了四肢新骨形成，组织病理学检查显示其减轻了滑膜炎、软骨侵蚀和骨质破坏。阿克他利抑制了小鼠耳部皮肤对CII的迟发型反应，但对血清抗CII抗体水平无影响。这些结果表明，阿克他利通过抑制对CII的迟发型超敏反应来抑制小鼠CII诱导性关节炎的发展。
