Evaluation of the effects of various anti-arthritic drugs on type II collagen-induced mouse arthritis model

Phadke, Kalindi; Fouts, Rebecca L.; Parrish, John E.; Butler, Larry G.

doi:10.1016/0162-3109(85)90059-1

Cited by 48 publications

(48 citation statements)

References 21 publications

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“…indomethacin). Thus, the mouse air pouch model described here would appear in many ways to offer advantages over more classical methods, including the type II collagen-induced arthritis model as recently reviewed by Phadke et al (1985).…”

Section: Discussionmentioning

confidence: 99%

A modified mouse air pouch model for evaluating the effects of compounds on granuloma induced cartilage degradation

Bottomley¹,

Griffiths²,

Rising³

et al. 1988

British J Pharmacology

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1 Employing rat femoral head cartilage implanted in a 6 day old mouse air pouch, the effects of inflammatory stimuli (i.e. cotton pellets, carrageenan, zymosan) on the loss of proteoglycan and collagen and granuloma formation have been studied. 2 Wrapping of the cartilage in cotton resulted in granuloma formation with accelerated loss of proteoglycan and collagen over the 14 day implantation period. The amount of loss increased with increasing weight of cotton. 3 The effects of different classes of anti-rheumatic drugs on granuloma formation and proteoglycan and collagen loss from cotton wrapped femoral head cartilage in the mouse air pouch have been studied. 4 Non-steroidal anti-inflammatory drugs (NSAIDs) had no influence on granuloma formation, but in general accelerated the rates of proteoglycan and collagen loss. 5 Dexamethasone and prednisolone significantly reduced granuloma formation and had a marked protective effect on cartilage breakdown. 6 Of the slow acting anti-rheumatic drugs examined, only gold sodium thiomalate (GSTM) and dapsone significantly decreased cartilage loss, with an accompanying modest decrease in granuloma formation. 7 The immunosuppressants cyclophosphamide and methotrexate, but not azathioprine, reduced cartilage degradation, but had no effect on granuloma formation. 8 The results for the different classes of anti-inflammatory and anti-rheumatic drugs are discussed in relation to their effects in other animal models and their reported therapeutic activities in man. It is concluded that the mouse air pouch method as described offers advantages as an animal model over existing procedures to predict therapeutic efficacy in man.

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Section: Discussionmentioning

confidence: 99%

A modified mouse air pouch model for evaluating the effects of compounds on granuloma induced cartilage degradation

Bottomley¹,

Griffiths²,

Rising³

et al. 1988

British J Pharmacology

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“…Similarly, the ability of chloroquine to inhibit arachidonic acid release with the concomitant inhibition ofthe prostaglandin cyclo-oxygenase-and lipoxygenase-derived arachidonic acid metabolites that are involved in inflammation (prostaglandins and leukotrienes) (Ford-Hutchinson et al, 1978;Higgs et al, 1979) may partly explain chloroquine-induced suppression ofinflammation (Tarayre et al, 1982;Phadke et al, 1982). Furthermore, chloroquine-induced inhibition of the vasodilator prostaglandins (PGI2 and PGE2) may partly contribute towards better understanding of the biochemical mechanisms that underly chloroquine-induced retinopathy and nephrotoxicity (Datsis, 1972;Converse, 1982).…”

Section: Discussionmentioning

confidence: 99%

“…Similarly, the antimalarial drug chloroquine (McChesney & Fitch, 1984) exerts anti-inflammatory activity in some models of inflammation (Palmer & Weatherall, 1977;Tarayre et al, 1982;Phadke et al, 1982). Since shistosomal infections are accompanied by intestinal and urinary bladder inflammation, and prostacyclin (PGI2) and other prostaglandins are known to mediate and/or potentiate inflammation (Ford-Hutchinson et al, 1978;Kunkel et al, 1981), it was thought of interest to examine the influences of the aforementioned drugs on PGI2 synthesis by rat arterial and myometrial tissues.…”

Section: Introductionmentioning

confidence: 99%

Influence of niridazole and chloroquine on arterial and myometrial prostacyclin synthesis

Tahir

1987

British J Pharmacology

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1 The effects of niridazole and chloroquine on rat arterial and myometrial prostacyclin (PGI2) synthesis in vitro were investigated by use of a rat platelet antiaggregatory bioassay. Niridazole (233 JtM) and chloroquine (97 pM) inhibited PGI2 synthesis in both tissues.2 Niridazole-induced inhibition in the myometrium was not reversed by exogenous arachidonic acid (33 JiM) indicating a direct effect of the compound on PGI2 synthesizing enzymes. 3 Chloroquine-induced inhibition in the myometrium was significantly reversed by exogenous arachidonic acid (33 pM) indicating a direct effect of the compound on arachidonic acid releasing enzymes (e.g. phospholipases A2 and C). 4 Niridazole and chloroquine also inhibited prostaglandin E2 synthesis in the myometrium. 5 Chloroquine-and niridazole-induced inhibition ofprostaglandin synthesis may contribute towards a better understanding of some of their actions in vivo.

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“…Both hind paws of each rat were dipped in a mercury bath and the volume of displacement of mercury was measured twice a week [12,13]. Along with the swelling of hind paws, visual disfigurement, restricted movement, and radiologic evaluation of the joints were taken into consideration to determine the degree of arthritis.…”

Section: Evaluation Of Inflammatory Responsementioning

confidence: 99%

Anti-Rheumatic Activity of Celecoxib and Methotrexate in Collagen Induced Arthritis: A Proteomic Approach

Baru¹,

Bitla²

2017

J Pharmacogenomics Pharmacoproteomics

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Rheumatoid Arthritis (RA) is a chronic inflammatory disorder of the synovial membrane that results in the destruction of bone and cartilage in affected joints. In order to identify novel disease-related proteins and candidate biomarkers, we analyzed the changes in the serum proteome profiles of rats with RA that were treated with a COX-2 inhibitor, celecoxib and a DMARD, methotrexate. Serum samples were collected from the RA rats before and after the drug treatment. Following immunodepletion of major proteins, the proteins were digested. The proteins were identified using MALDI-TOF mass spectrometry. Several proteins are identified and the proteins that play a key role in RA are studied. These proteins are inhibited differentially by celecoxib and methotrexate. Although some of the proteins are known to be related to RA, several are currently unknown with respect to their relationship to RA and may be involved in the development of this disease. Our results may contribute to the identification of novel disease related proteins and enhance the understanding of the pathogenesis of RA.

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Evaluation of the effects of various anti-arthritic drugs on type II collagen-induced mouse arthritis model

Cited by 48 publications

References 21 publications

A modified mouse air pouch model for evaluating the effects of compounds on granuloma induced cartilage degradation

A modified mouse air pouch model for evaluating the effects of compounds on granuloma induced cartilage degradation

Influence of niridazole and chloroquine on arterial and myometrial prostacyclin synthesis

Anti-Rheumatic Activity of Celecoxib and Methotrexate in Collagen Induced Arthritis: A Proteomic Approach

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