Ueno M, Imaizumi K, Sugita T, Takata I, Takeshita M
Research Laboratory of Applied Biochemistry, Tanabe Seiyaku Co., Ltd, Osaka, Japan.
Int J Immunopharmacol. 1995 Jul;17(7):597-603. doi: 10.1016/0192-0561(95)00057-9.
The effects of Ta-383 (0.016, 0.08, 0.4, 2 and 10 mg/kg) and anti-rheumatic drugs (lobenzarit 10 and 50 mg/kg, dexamethasone 0.25 mg/kg) were evaluated on type II collagen-induced arthritis in DBA/1J mice. The arthritis score was markedly suppressed in the groups treated with dexamethasone and TA-383. Serum anti-type II collagen IgG was significantly suppressed in the groups treated with dexamethasone and 0.4 mg/kg TA-383. Histopathological evaluation of the knee joints revealed suppression of the inflammatory changes in the groups treated with dexamethasone and TA-383. These findings suggest that the histopathological examination of the joints of the animal model is useful for the evaluation of anti-rheumatic drugs, and that TA-383 has suppressive effects on type II collagen-induced arthritis, an animal model for human rheumatoid arthritis.
评估了Ta - 383（0.016、0.08、0.4、2和10毫克/千克）和抗风湿药物（氯苯扎利10和50毫克/千克、地塞米松0.25毫克/千克）对DBA/1J小鼠II型胶原诱导性关节炎的影响。地塞米松和Ta - 383治疗组的关节炎评分明显受到抑制。地塞米松和0.4毫克/千克Ta - 383治疗组的血清抗II型胶原IgG显著受到抑制。膝关节的组织病理学评估显示，地塞米松和Ta - 383治疗组的炎症变化受到抑制。这些发现表明，动物模型关节的组织病理学检查有助于评估抗风湿药物，并且Ta - 383对II型胶原诱导性关节炎（一种人类类风湿性关节炎的动物模型）具有抑制作用。
