Ochi Takehiro, Goto Toshio
Department of Immunology and Inflammation, Medicinal Biology Research Laboratories, Fujisawa Pharmaceutical Co., Ltd., 1-6, Kashima 2-chome, Yodogawa-ku, Osaka, 532-8514, Japan.
Br J Pharmacol. 2002 Feb;135(3):782-8. doi: 10.1038/sj.bjp.0704511.
We investigated the effects of FR122047 (1-[(4,5-bis(4-methoxyphenyl)-2-thiazoyl)carbonyl]-4-methylpiperazine hydrochloride), a selective cyclo-oxygenase (COX)-1 inhibitor, in rat type II collagen-induced arthritis (CIA) and adjuvant-induced arthritis (AIA). Using an ex vivo rat whole blood assay, FR122047 (0.032 - 3.2 mg kg(-1)) inhibited COX-1-derived thromboxane (TX) B(2) production with ED(50) value of 0.059 mg kg(-1), indicating that it was orally active, but did not inhibit lipopolysaccharide-induced prostaglandin (PG) E(2) production derived by COX-2. Oral administration of FR122047 showed a dose-dependent anti-inflammatory effect in rat CIA with ED(50) value of 0.56 mg kg(-1). This drug also dose dependently suppressed the levels of PGE(2) and TXB(2) in CIA rat paws with ED(50) values of 0.24 and 0.13 mg kg(-1), respectively. FR122047 had no effect in rat AIA model. In contrast, indomethacin, a non-selective COX inhibitor, was anti-inflammatory and reduced the formation of PGs in AIA rat paws. Unlike indomethacin, chronic treatment of FR122047 did not damage the stomach mucosa in CIA rats. These results demonstrate that COX-1 contributes to the oedema and the formation of PGE(2) and TXB(2) in rat CIA model, but not in rat AIA model. We conclude that FR122047 has an orally active and anti-inflammatory effect mediated by inhibition of PGE(2) and TXB(2) produced by COX-1 at a site of inflammation induced by type II collagen and it may be a useful tool for studying the involvement of COX-1 in various in vivo models of inflammation.
我们研究了选择性环氧化酶(COX)-1抑制剂FR122047(1-[(4,5-双(4-甲氧基苯基)-2-噻唑基)羰基]-4-甲基哌嗪盐酸盐)对大鼠II型胶原诱导性关节炎(CIA)和佐剂诱导性关节炎(AIA)的影响。采用大鼠全血体外试验,FR122047(0.032 - 3.2 mg kg(-1))抑制COX-1衍生的血栓素(TX)B(2)生成,ED(50)值为0.059 mg kg(-1),表明其口服具有活性,但不抑制脂多糖诱导的COX-2衍生的前列腺素(PG)E(2)生成。口服FR122047在大鼠CIA中显示出剂量依赖性抗炎作用,ED(50)值为0.56 mg kg(-1)。该药物还剂量依赖性地抑制CIA大鼠爪中PGE(2)和TXB(2)水平,ED(50)值分别为0.24和0.13 mg kg(-1)。FR122047在大鼠AIA模型中无作用。相比之下,非选择性COX抑制剂吲哚美辛具有抗炎作用,并减少AIA大鼠爪中PG的形成。与吲哚美辛不同,FR122047的长期治疗不会损伤CIA大鼠的胃黏膜。这些结果表明,COX-1在大鼠CIA模型中促成水肿以及PGE(2)和TXB(2)的形成,但在大鼠AIA模型中并非如此。我们得出结论,FR122047通过抑制II型胶原诱导的炎症部位COX-1产生的PGE(2)和TXB(2)而具有口服活性和抗炎作用,它可能是研究COX-1在各种体内炎症模型中作用的有用工具。