The effect of TRK-530 on experimental arthritis in mice

Biol Pharm Bull. 1997 Nov;20(11):1147-50. doi: 10.1248/bpb.20.1147.


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-1 beta in vitro was studied. TRK-530 at a concentration of 10(-4) M inhibited LPS-induced IL-1 beta 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-1 beta production may partly participate the anti-rheumatoid action of TRK-530.

MeSH terms

  • Animals
  • Antibody Formation
  • Arthritis / drug therapy*
  • Arthritis / etiology
  • Arthritis / immunology
  • Collagen / adverse effects
  • Diphosphonates / therapeutic use*
  • Hypersensitivity, Delayed
  • Immunity, Cellular
  • Interleukin-1 / biosynthesis
  • Male
  • Mice
  • Mice, Inbred DBA


  • Diphosphonates
  • Interleukin-1
  • TRK 530
  • Collagen