Ueno M, Sugita T, Murakami T, Takata I
Lead Generation Research Laboratory, Tanabe Seiyaku Co., Ltd., Osaka, Japan.
Jpn J Pharmacol. 1997 Jun;74(2):221-4. doi: 10.1254/jjp.74.221.
We have investigated the effect of a novel anti-rheumatic drug, cis-2-(4-chlorophenyl)-4,5-diphenyl-2-imidazoline hydrochloride (TA-383), on macrophages. TA-383 (> or = 10(-9) M) significantly stimulated rabbit alveolar macrophage (AM) migration, and its migration-stimulatory activity was more potent than those of L-fucose (5 x 10(-3) M), lobenzarit disodium, bucillamine (SA-96) and salazosulfapyridine. In addition, TA-383 enhanced the production and/or release of macrophage migration enhancement factor by rabbit spleen cells. In vivo, TA-383 (0.4 mg/kg, p.o.) has suppressive effects on picryl chloride-induced delayed type hypersensitivity and type II collagen-induced arthritis in mice. These results suggest that the anti-rheumatic activity of TA-383 may be exerted through the dispersion of macrophages from inflammatory sites.
我们研究了一种新型抗风湿药物顺式-2-(4-氯苯基)-4,5-二苯基-2-咪唑啉盐酸盐（TA-383）对巨噬细胞的作用。TA-383（≥10⁻⁹ M）显著刺激兔肺泡巨噬细胞（AM）迁移，其迁移刺激活性比L-岩藻糖（5×10⁻³ M）、氯苯柳胺二钠、布西拉明（SA-96）和柳氮磺胺吡啶更强。此外，TA-383增强了兔脾细胞巨噬细胞迁移增强因子的产生和/或释放。在体内，TA-383（0.4 mg/kg，口服）对小鼠皮内注射氯化苦诱导的迟发型超敏反应和Ⅱ型胶原诱导的关节炎具有抑制作用。这些结果表明，TA-383的抗风湿活性可能是通过将巨噬细胞从炎症部位驱散来发挥的。
