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  • 标题:The Effect of TRK-530 on Experimental Arthritis in Mice
  • 本地全文:下载
  • 作者:Yuko TAKAOKA ; Hiroichi NAGAI ; Hiroshi MORI
  • 期刊名称:Biological and Pharmaceutical Bulletin
  • 印刷版ISSN:0918-6158
  • 电子版ISSN:1347-5215
  • 出版年度:1997
  • 卷号:20
  • 期号:11
  • 页码:1147-1150
  • DOI:10.1248/bpb.20.1147
  • 出版社:The Pharmaceutical Society of Japan
  • 摘要:TRK-530 is a newly synthesized diphosphonate derivative. We investigated the effect of TRK-530 on type II collagen-induced arthritis (CIA) in mice in comparison to that of prednisolone and indomethacin. TRK-530 at a dose of 25 mg/kg showed a tendency to inhibit CIA. TRK-530 at a dose of 50 mg/kg inhibited the development of the CIA in terms of the progression of footpad swelling, bone damage and histopathological changes. TRK-530 at a dose of 50 mg/kg also significantly inhibited the delayed type hypersensitivity (DTH) response to type II collagen, but not the production of anti-type II collagen IgG antibody in arthritic mice.To investigate the inhibitory mechanism of TRK-530, the type of effect of TRK-530 on the production of IL-1β in vitro was studied. TRK-530 at a concentration of 10-4M inhibited LPS-induced IL-1β production from J774.1 cells.In conclusion, TRK-530 inhibited CIA in mice. The inhibition of the DTH reaction to type II collagen and the inhibition of IL-1β production may partly participate the anti-rheumatoid action of TRK-530.
  • 关键词:TRK-530;collagen-induced arthritis;interleukin-1β (IL-1β)
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