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Publications (5)3.53 Total impact

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    ABSTRACT: The anti-inflammatory effects of etodolac (Eto) were compared with those of 6 other anti-inflammatory drugs: indomethacin (Ind), diclofenac Na (Dic), piroxicam (Pir), naproxen (Nap), ketoprofen (Ket) and aspirin (Asp). Eto inhibited carrageenin-induced edema in rats, adjuvant-induced arthritis in rats, acetic acid-induced writhing in mice and brewer's yeast-induced hyperalgesia and fever in rats. In the adjuvant arthritis test, the ED30 value (1.88 mg/kg) on day 3 and ED50 values (adjuvant-injected paw: 1.18 mg/kg and non-injected paw: 0.96 mg/kg) on day 18 for Eto were comparable to those for Dic (2.16, 1.72 and 1.28) when given prophylactically and the ED50 values for Eto (adjuvant-injected paw: 1.61 and non-injected paw: 1.20 mg/kg) were comparable to those for Ket (1.24 and 1.22) when used therapeutically. The analgesic activity of Eto (ED50 value: 3.67 mg/kg) in the acetic acid-induced writhing test was greater than that of Nap (9.83) or Asp (31.6) and less than that of Ind (0.71), Dic (1.54), Pir (0.92) or Ket (1.34). In the antipyretic test, the minimum effective dose (MED: 1 mg/kg) for Eto was comparable to that for Ind (1.0), Nap (1.0) or Ket (1.0). Eto was less potent in inhibiting carrageenin-induced edema (ED30 value: 6.99 mg/kg) and inflammatory pain (ED50 value: 9.24 mg/kg) than the other drugs (Ind: 2.32 and 3.47, Dic: 0.69 and 3.80, Pir: 1.31 and 1.94, Nap: 1.83 and 2.78, Ket: 1.12 and 0.63), except for Asp (167 and 51.8).(ABSTRACT TRUNCATED AT 250 WORDS)
    Biological & Pharmaceutical Bulletin 01/1995; 17(12):1577-83. · 1.85 Impact Factor
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    ABSTRACT: The effect of actarit (MS-932, CAS 18699-02-0), an antirheumatic drug, on type II collagen (CII)-induced arthritis in DBA/1J mice was studied. Mice were immunized twice with bovine CII, actarit being given orally once a day for 35 days after the 1st immunization. Clinical assessment showed that actarit had no effect on the incidence or day of onset of arthritis but that it lowered the arthritis score dose-dependently. Radiography showed that actarit reduced new bone formation in the limbs, and a histopathologic examination showed that it reduced synovitis, erosion of cartilage and bone destruction. Actarit suppressed the delayed-type mouse ear skin reaction to CII but had no effect on the level of serum anti-CII antibodies. These results suggest that actarit inhibits the development of CII-induced arthritis in mice by suppressing delayed-type hypersensitivity to CII.
    Arzneimittel-Forschung 02/1994; 44(1):64-8. · 0.56 Impact Factor
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    ABSTRACT: We tested the effect of etodolac on the development of type-II collagen-induced arthritis in DBA/1J mice. It was administered orally once daily for 35 days after the primary immunization with type-II collagen. Etodolac (10 mg/kg) significantly inhibited the development of signs of arthritis on day 28 to day 35. Indomethacin (1 mg/kg) also significantly inhibited it on day 29 to day 34. Radiographic examination showed that etodolac (10 mg/kg) significantly prevented the development of osteopenia, bone erosion and new bone formation of the joints on day 35, while indomethacin (1 mg/kg) significantly prevented only the development of bone erosion. Histopathological examination showed that both etodolac (10 mg/kg) and indomethacin (1 mg/kg) significantly prevented the development of synovitis, erosion of cartilage of the joints and bone destruction of the limbs on day 35. Etodolac and indomethacin did not affect the serum level of anti-type-II collagen antibodies. These results suggest that etodolac and indomethacin suppress type-II collagen-induced arthritis without affecting humoral immune responses.
    Agents and Actions 08/1993; 39(3-4):187-94.
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    ABSTRACT: The anti-inflammatory, analgesic, antipyretic and ulcerogenic activities of etodolac (CAS 41340-25-4), a new nonsteroidal anti-inflammatory agent, were compared with those of indometacin and other anti-inflammatory drugs in experimental animals. Etodolac had a remarkable anti-inflammatory effect in various experimental models: ultraviolet erythema, carrageenin-induced edema and swelling of adjuvant arthritis. In these models, the effective dose of etodolac was several fold that of indometacin. Etodolac inhibited prostaglandin E2 formation in a concentration-dependent manner, and its inhibitory potency was about 1/5 of that of indometacin. Etodolac also caused marked inhibition of granuloma formation and leucocyte functions such as chemotaxis, lysosomal enzyme release and active oxygen generation. These effects of etodolac were observed at similar doses of indometacin. Etodolac suppressed inflammatory pain but not non-inflammatory pain, and had an antipyretic effect but did not lower normal rectal temperature. Etodolac had no effect on delayed hypersensitivity reactions and was much less ulcerogenic than indometacin. These results indicate that etodolac is a low ulcerogenic anti-inflammatory agent with suppressing activities on leucocyte functions to the same extent as indometacin and prostaglandin biosynthesis.
    Arzneimittel-Forschung 04/1991; 41(3):228-35. · 0.56 Impact Factor
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    ABSTRACT: The effect of etodolac (CAS 41340-25-4) on the inflammatory reactions induced by histamine and bradykinin was compared with that of indomethacin and other nonsteroidal anti-inflammatory drugs. Etodolac (50 mg/kg p.o.), indomethacin (20 mg/kg p.o.), diclofenac Na (20 mg/kg p.o.) and acetylsalicylic acid (200 mg/kg p.o.) had no effect on the increase of vascular permeability induced by histamine or bradykinin and on passive cutaneous anaphylaxis in rats. Etodolac (5, 10 and 20 mg/kg p.o.) suppressed concanavalin A-induced paw edema in rats. Etodolac (10 mg/kg p.o.) and bromelain (10 mg/kg i.v.) significantly suppressed the heat-induced elevation of bradykinin in perfusates of rat paws, but indomethacin (20 mg/kg p.o.) and diclofenac Na (20 mg/kg p.o.) did not. Etodolac inhibited bradykinin-forming enzyme activity in a concentration-dependent manner (IC50 = 1.5 x 10[-4) mol/l). These results suggest that etodolac is a unique nonsteroidal anti-inflammatory drug which can inhibit bradykinin formation, unlike indomethacin or diclofenac Na.
    Arzneimittel-Forschung 04/1991; 41(3):235-9. · 0.56 Impact Factor