Pathological Evaluation of Anti-rheumatic Drugs on Type II Collagen-induced Arthritis in DBA/1J Mouse

Imaizumi, Kazunori; Hinoue, Hiromi; Ueno, Masashi; Takata, Isao; Satô, Tadashi; Minato, Yoshio; Takeshita, Masakazu; Okaniwa, Azusa

doi:10.1538/expanim1978.40.1_95

Cited by 4 publications

(2 citation statements)

References 11 publications

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“…Auranofin 9) and D-penicillamine 10) increase the severity of the arthritis and/or accelerate its onset. Lobenzarit 11) is not effective in CIA model.…”

Section: Discussionmentioning

confidence: 91%

Effect of (3,5,6-Trimethylpyrazin-2-yl)methyl 2-[4-(2-Methylpropyl)-phenyl] propanoate (ITE), a Newly Developed Anti-inflammatory Drug, on Type II Collagen-Induced Arthritis in Mice

Cao

et al. 2004

Biological & Pharmaceutical Bulletin

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Type II collagen (CII)-induced arthritis (CIA) in rats 1) and mice 2) has both clinical and histological similarities to human rheumatoid arthritis.1-4) Trentham 1) suggested that an immune reaction to collagen may be involved in the pathogenesis of arthritis. The CIA model has been widely used to evaluated antiarthritic drugs.5-7) ITE (3,5,6-trimethylpyrazin-2-yl)methyl 2-[4-(2-methylpropyl)phenyl]propanoate ( Fig. 1), is a newly developed anti-inflammatory drug.8) In the present study the effect of ITE on CIA in mice and its effect on immune responses to CII in CIA mice were evaluated. MATERIALS AND METHODS AnimalsMale Kun-ming mice weighing 18-22 g were purchased from Shenyang Pharmaceutical University Laboratory Animal Center. Mice were housed in a room under a 12 h light-dark cycle and quarantined for one week before use. The mice were given standard laboratory chow and tap water ad libitum.Drugs ITE synthesized at Hua-tai Institute of Pharmaceutics Science was used. ITE occurs as white powder. Purity of ITE is more than 98.5%. ITE (150, 300, 600 mg/kg) or ibuprofen (IB, 180 mg/kg) was suspended in a 0.5% carboxymethylcellulose (CMC)-saline solution and given orally to mice once a day for 40 d from the day of 1st immunization with CII. Mice in the control group were orally given 0.5% CMC-saline. Type II collagen were purchased from Sigma Co. (St. Louis, U.S.A.). Induction of Arthritis 7)CII was dissolved overnight at 4°C in 0.1 M acetic acid at 2 mg/ml, after which the solution was emulsified in an equal volume of complete Freund's adjuvant (CFA). This emulsion containing 100 mg of CII was injected intradermally into the base of the tail, and the mice were given an intraperitoneal injection of the same emulsion 20 d later.Clinical Assessment 7)The clinical symptoms of arthritis in limbs were evaluated blindly with a visual scoring system every 4 d after day 20. Arthritic lesion of a limb was graded on a scale of 0-4: 0ϭno change, 1ϭswelling and erythema of the digit, 2ϭmild swelling and erythema of the limb, 3ϭgross swelling and erythema of the digit, 4ϭgross deformity and inability to use the limb. The arthritis score of each mouse was the sum of the scores of each of the limbs except the right hind limb, the maximum score being 12. A mouse that showed a score of 1 or more was regarded to be arthritic. The incidence and day of onset of arthritis also were recorded. The right hind paw's volume of each mouse was determined on days 0, 20, 24, 28, 32, 36 and 40 after 1st immunization with CII. Measurement of Anti-CII Antibodies 7)On day 40, blood was collected from the mice, after which the serum level of IgG antibodies to CII was determined by the enzyme-linked immunosorbent assay (ELISA). Briefly a 100 ml sample of serum (1 : 2000) in phosphate-buffered saline (PBS) was added to the wells of a 96 well plate that had been coated with CII overnight at 4°C. The plate was incubated for 2 h at room temperature then, after the washing of the wells with PBS, an addition was made of 100 ml goat antimouse IgG (1 : 40...

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“…Auranofin 9) and D-penicillamine 10) increase the severity of the arthritis and/or accelerate its onset. Lobenzarit 11) is not effective in CIA model.…”

Section: Discussionmentioning

confidence: 91%

Effect of (3,5,6-Trimethylpyrazin-2-yl)methyl 2-[4-(2-Methylpropyl)-phenyl] propanoate (ITE), a Newly Developed Anti-inflammatory Drug, on Type II Collagen-Induced Arthritis in Mice

Cao

et al. 2004

Biological & Pharmaceutical Bulletin

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“…Previ ously, we reported the histopathological characteristics of arthritic lesions and pathological evaluation of the effects of anti-rheumatoid drugs on collagen-induced arthritis in DBA/1J mice [8,9].…”

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confidence: 99%

Histopathological Study of Arthritic Lesions Induced by Immunization with Type II Collagen in Lewis Rats

Imaizumi¹,

Hinoue

Ueno

et al. 1994

Experimental Animals

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Complete prevention of the clinical expression of adjuvant-induced arthritis in rats by cyclosporin-A and lobenzarit: The regulation of lymph node cell populations and cytokine production

et al. 1996

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A single dose of either cyclosporin-A (CsA) or lobenzarit (CCA) given with an arthrogenic adjuvant completely prevented expression of experimental adjuvant arthritis in rats. The aim of this study was to understand how these drugs prevented the arthritis expression by studying the popliteal lymph nodes draining the arthritic joints at various times after adjuvant injection. Neither drug affected the proliferation in popliteal lymph nodes at the time arthritis was normally expressed, however, there was a marked change in the types of cells present. Immunofluorescence assays showed a reduction in the proportion of CD4+ cells, while the proportion of B-lymphocytes was almost doubled. This coincided with a marked elevation in the ability of these cells to produce interleukin (IL)-6. At the same time production of other cytokines (IL-2, tumour necrosis factor (TNF) and interferon (IFN)-gamma) was not greatly affected. However, one day after adjuvant injection IL-2 and IFN-gamma production was reduced. In vitro experiments showed that IL-6 production by lymphoid cells was relatively unaffected by CsA and CCA but IL-2, TNF and IFN-gamma were suppressed by CsA. The results indicate that CsA and CCA may modify the response to the arthritic adjuvant by specifically inhibiting IL-2, TNF and IFN-gamma production at the time of adjuvant injection. The lack of inhibition of IL-6 by these drugs reveals it may not play a key role in the initiation of this model of chronic inflammation.

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Pathological Evaluation of Anti-rheumatic Drugs on Type II Collagen-induced Arthritis in DBA/1J Mouse

Cited by 4 publications

References 11 publications

Effect of (3,5,6-Trimethylpyrazin-2-yl)methyl 2-[4-(2-Methylpropyl)-phenyl] propanoate (ITE), a Newly Developed Anti-inflammatory Drug, on Type II Collagen-Induced Arthritis in Mice

Effect of (3,5,6-Trimethylpyrazin-2-yl)methyl 2-[4-(2-Methylpropyl)-phenyl] propanoate (ITE), a Newly Developed Anti-inflammatory Drug, on Type II Collagen-Induced Arthritis in Mice

Histopathological Study of Arthritic Lesions Induced by Immunization with Type II Collagen in Lewis Rats

Complete prevention of the clinical expression of adjuvant-induced arthritis in rats by cyclosporin-A and lobenzarit: The regulation of lymph node cell populations and cytokine production

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