Pathological Evaluation of Effect of Anti-rheumatic Drugs on Type II Collagen-induced Arthritis in Lewis Rats.

Abstract

The effects of anti-rheumatic drugs (dexamethasone 0.1 mg/kg and naproxen 5 mg/kg) were evaluated immunologically and histopathologically on type II collagen-induced arthritis in Lewis rats. Increased paw volume in the hind limbs was significantly suppressed in the groups treated with dexamethasone or naproxen, but noticeable retardation of body weight gain was observed in the group treated with dexamethasone. Serum anti-type II collagen IgG was significantly suppressed in the group treated with dexamethasone but not naproxen. Histopathological evaluation by our grading system, classification of the stages in arthritic lesion development, revealed suppression of the inflammatory changes in the tarsal joints of the animals treated with dexamethasone or naproxen. From our results, histopathological evaluation is considered to be more suitable for assessment of the efficacy of anti-rheumatic drugs on type II collagen-induced arthritis, an animal model for human rheumatoid arthritis.

Modeling Sex Differences in Pharmacokinetics, Pharmacodynamics, and Disease Progression Effects of Naproxen in Rats with Collagen-Induced Arthritis

“…The absorption of NPX from the intraperitoneal injection site was rapid (k a of approximately 1 h 21 ). Arthritic rats showed lower unbound plasma clearance of NPX (1438 ml/h per kg) compared with healthy rats (1968 ml/h per kg), which is in accordance with findings in humans (van den Ouweland et al, 1987). The estimated tissue distribution rate of NPX was much lower (f d = 0.15) than the cardiac plasma flow (when f d = 1), which is in line with the permeabilitylimited distribution of NPX, as it is a highly ionized drug.…”

Differential effect of FR122047, a selective cyclo‐oxygenase‐1 inhibitor, in rat chronic models of arthritis

“…It is well known that adjuvant‐induced arthritis (AIA) and type II collagen‐induced arthritis (CIA) are animal models of rheumatoid arthritis for detecting new anti‐rheumatic drugs (Bartlett & Schleyerbach, 1985; Takeoka et al ., 1993). In these rheumatoid models, non‐steroidal anti‐inflammatory drugs (NSAIDs) have been reported to reduce development of arthritis (Bendele et al ., 1992; Takeshita et al ., 1997). NSAIDs inhibit the formation of prostaglandins (PGs) which are important lipid mediators of the inflammatory process and are products of the cyclo‐oxygenase (COX) pathway of arachidonic acid metabolism (Vane, 1971).…”

Regulation of cell proliferation, inflammatory cytokine production and calcium mobilization in primary human T lymphocytes by emodin from Polygonum hypoleucum Ohwi

“…The production of cytokines such as interleukin-2 (IL-2) and IL-4 is pivotal in the growth of T lymphocytes induced by antigens or phytohemagglutinin (PHA) [16]. In patients with arthritis, the levels of inflammatory cells, T cells and cytokines have been shown to be significantly elevated in the synovial tissue or synovial fluid, suggesting a possible pathological role for these cells and substances [17]. One of the therapeutic objectives in arthritis is to reduce the local inflammatory response by diminishing the inflammatory cell activation and proliferation, as well as the inflammatory cytokine production.…”